As our understanding of the underlying aetiology of hypertension is far from adequate, over 90% of patients with hypertension receive a diagnosis of essential hypertension. This non-specific diagnosis leads to suboptimal therapeutics and a major problem with non-compliance. Understanding the normal control of blood pressure (BP) is, hence, important for a better understanding of the disease.This review attempts to unravel the present understanding of BP control. The local mechanisms of BP control, the neural mechanisms, renal-endocrine mechanisms, and a variety of other hormones that have a bearing in normal BP control are discussed and the possible role in the pathophysiology is alluded to.

Aging is increasingly regarded as an independent risk factor for development of cardiovascular diseases such as atherosclerosis and hypertension and their complications (e.g. MI and Stroke). It is well known that vascular disease evolve over decades with progressive accumulation of cellular and extracellular materials and many inflammatory processes. Metabolic syndrome, obesity and diabetes are conventionally recognized as risk factors for development of coronary vascular disease (CVD). These conditions are known to accelerate ageing process in general and vascular ageing in particular. Adverse events during intrauterine life may programme organ growth and favour disease later in life, popularly known as, 'Barker's Hypothesis'. The notion of fetal programming implies that during critical periods of prenatal growth, changes in the hormonal and nutritional milieu of the conceptus may alter the full expression of the fetal genome, leading to permanent effects on a range of physiological.

Hypertension affects about 10 - 25% of the population and is an important risk factor for cardiovascular and renal disease. The renin-angiotensin system is frequently implicated in the pathophysiology of hypertension, be it primary or secondary. The prevalence of primary aldosteronism increases with the severity of hypertension, from 2% in patients with grade 1 hypertension to 20% among resistant hypertensives. Mineralcorticoid hypertension includes a spectrum of disorders ranging from renin-producing pathologies (renin-secreting tumors, malignant hypertension, coarctation of aorta), aldosterone-producing pathologies (primary aldosteronism - Conns syndrome, familial hyperaldosteronism 1, 2, and 3), non-aldosterone mineralocorticoid producing pathologies (apparent mineralocorticoid excess syndrome, Liddle syndrome, deoxycorticosterone-secreting tumors, ectopic adrenocorticotropic hormones (ACTH) syndrome, congenitalvadrenal hyperplasia), and drugs with mineraocorticoid activity (locorice, carbenoxole therapy) to glucocorticoid receptor resistance syndromes. Clinical presentation includes hypertension with varying severity, hypokalemia, and alkalosis. Ratio of plasma aldosterone concentraion to plasma renin activity remains the best screening tool. Bilateral adrenal venous sampling is the best diagnostic test coupled with a CT scan. Treatment is either surgical (adrenelectomy) for unilateral adrenal disease versus medical therapy for idiopathic, ambiguous, or bilateral disease. Medical therapy focuses on blood pressure control and correction of hypokalemia using a combination of anti-hypertensives (calcium channel blockers, angiotensin converting enzyme inhibitors, or angiotensin receptor blockers) and potassium-raising therapies (mineralcorticoid receptor antagonist or potassium sparing diuretics). Direct aldosterone synthetase antagonists represent a promising future therapy.

Hypertension is a major and frequent comorbid finding of Cushing's syndrome. This review discusses the etiology and pathophysiology of hypertension in Cushing's syndrome, while suggesting methods of management of this condition. It also provides an overview of diagnosis and management strategies in this disease.

The projected prevalence of Cushing's syndrome (CS) inclusive of subclinical cases in the adult population ranges from 0.2-2% and it may no longer be considered as an orphan disease (2-3 cases/million/year). The recognition of CS by physicians is important for early diagnosis and treatment. Late-night salivary cortisol, dexamethasone suppressiontesti, or 24-h urine free cortisol are good screening tests. Positively screened cases need stepwise evaluation by an endocrinologist. This paper discusses the importance of screening for CS and suggests a stepwise diagnostic approach to a case of suspected hypercortisolism.

Cushing's syndrome is a clinical situation, caused by excessive glucocorticoid level, resulting in several features such as central obesity, supraclavicular fat, "moon face," "buffalo hump," hyperglycemia, metabolic alkalosis, hypokalemia, poor wound healing, easy bruising, hypertension, proximal muscle weakness, thin extremities, skin thinning, menstrual irregularities, and purple striae. In the perioperative period, the anesthesiologist must deal with difficult ventilation and intubation, hemodynamic disturbances, volume overload and hypokalemia, glucose intolerance, and diabetes, maintaining the blood cortisol level and preventing the glucocorticoid deficiency. This syndrome is quite rare and its features make these patients very difficult to the anesthesiologist.

Pheochromocytoma is a rare tumor arising from chromaffin cells in adrenal medulla or other paraganglia in the body, which may be associated with many genetic syndromes and mutation. The role of endocrinologist is in biochemical diagnosis of suspected cases; its anatomic and functional localization with the help of imaging like CT, MRI, and nuclear scanning; preoperative control of hypertension; and postoperative follow-up of cases that have undergone surgical resection. Familial and genetic screening of cases and their family is important to detect occult cases. Endocrinologist will also play a role in cases with malignant pheochromocytoma in assessment of metastasis, control, chemoradiotherapy, and follow-up.

Pheochromocytoma is a rare catecholamine secreting tumor arising commonly from adrenal medulla. It has got multidimensional challenging aspects in spite of our improved understanding of its physiological and clinical behavior during surgical resection. This neuroendocrine tumor is associated with a most unpredictable and fluctuating clinical course during anesthesia and surgical intervention. The clinical difficulties and challenges increase manifold in patients with undiagnosed or accidental diagnosis of pheochromocytoma who present to the hospital for the treatment of some other disease or emergency. The most common manifestations of this clinical spectrum include hypertension, headache, palpitations, episodic sweating, and feeling of doom. The definite and only treatment for this rare tumor is surgical resection which itself is very challenging for an anesthesiologist. This article reviews the pre-operative evaluation, pharmacological preparation, intraoperative and post-operative management of patients with pheochromocytoma especially from anesthesiologist's perspectives.

Natriuretic peptides (NPs) are hormones which are mainly secreted from heart and have important natriuretic and kaliuretic properties. There are four different groups NPs identified till date [atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP), C-type natriuretic peptide (CNP) and dendroaspis natriuretic peptide, a D-type natriuretic peptide (DNP)], each with its own characteristic functions. The N-terminal part of the prohormone of BNP, NT-proBNP, is secreted alongside BNP and has been documented to have important diagnostic value in heart failure. NPs or their fragments have been subjected to scientific observation for their diagnostic value and this has yielded important epidemiological data for interpretation. However, little progress has been made in harnessing the therapeutic potential of these cardiac hormones.

Thyroid disorders and primary hyperparathyroidism have been known to be associated with increases in blood pressure. The hypertension related to hypothyroidism is a result of increased peripheral resistance, changes in renal hemodynamics, hormonal changes and obesity. Treatment of hypothyroidism with levo-thyroxine replacement causes a decrease in blood pressure and an overall decline in cardiovascular risk. High blood pressure has also been noted in patients with subclinical hypothyroidism. Hyperthyroidism, on the other hand, is associated with systolic hypertension resulting from an expansion of the circulating blood volume and increase in stroke volume. Increased serum calcium levels associated with a primary increase in parathyroid hormone levels have been also associated with high blood pressure recordings. The mechanism for this is not clear but the theories include an increase in the activity of the renin-angiotensin-aldosterone system and vasoconstriction. Treatment of primary hyperparathyroidism by surgery results in a decline in blood pressure and a decrease in the plasma renin activity. Finally, this review also looks at more recent evidence linking hypovitaminosis D with cardiovascular risk factors, particularly hypertension, and the postulated mechanisms linking the two.

Endocrine causes of hypertension are rare in children and screening for endocrine hypertension in children should be carried out only after ruling out renal and renovascular causes. Excess levels and/or action of mineralocorticoids associated with low renin levels lead to childhood hypertension and this can be caused by various conditions which are discussed in detail in the article. Childhood pheochromocytomas are being increasingly diagnosed because of the improved application of genetic testing for familial syndromes associated with pheochromocytomas. Adolescents with polycystic ovarian syndrome (PCOS) can also have hypertension associated with their obese phenotype.

Essential hypertension is the most common form of hypertension in adults, and it is recognized more often in adolescents than in younger children. It is well known that the probability of a diagnosis of essential hypertension increases with age from birth onward. The initiation of high blood pressure burden starts in childhood and continues through adolescence to persist in the remaining phases of life. The genesis of essential hypertension is likely to be multifactorial. Obesity, insulin resistance, activation of sympathetic nervous system, sodium homeostasis, renin-angiotensin system, vascular smooth muscle structure and reactivity, serum uric acid levels, genetic factors and fetal programming have been implicated in this disorder. In addition, erythrocyte sodium transport, the free calcium concentration in platelets and leukocytes, urine kallikrein excretion, and sympathetic nervous system receptors have also been investigated as other possible mechanisms. Obesity in children appears to be the lead contributor of essential hypertension prevalence in children and adolescents. Suggested mechanisms of obesity-related hypertension include insulin resistance, sodium retention, increased sympathetic nervous system activity, activation of renin-angiotensin-aldosterone, and altered vascular function. The etiopathogenesis of essential hypertension in children and adolescents appears to closely resemble that of adults. The minor variations seen could probably be due to the evolving nature of this condition. Many of the established mechanisms that are confirmed in adult population need to be replicated in the pediatric age group by means of definitive research for a better understanding of this condition in future.

Hypertension occurs twice as commonly in diabetics than in comparable nondiabetics. Patients with both disorders have a markedly higher risk for premature microvascular and macrovascular complications. Aggressive control of blood pressure (BP) reduces both micro- and macrovascular complications. In diabetic hypertensives, angiotensin converting enzyme inhibitors (ACEIs) are the first line in management of hypertension, and can be replaced by angiotensin II receptor blockers (ARBs) if patients are intolerant of them. Recent studies suggest ARBs to be on par with ACEI in reducing both macro- and microvascular risks. Adding both these agents may have a beneficial effect on proteinuria, but no extra macrovascular risk reduction. Thiazides can also be used as first line drugs, but are better used along with ACEI/ARBs. Beta-blockers [especially if the patient has coronary artery disease] and calcium channel blockers are used as second line add-on drugs. Multidrug regimens are commonly needed in diabetic hypertensives. Achieving the target BP of <130/80 is the priority rather than the drug combination used in order to arrest and prevent the progression of macro- and microvascular complications in diabetic hypertensives.

Hypertension is the most common medical disorder complicating pregnancy. However, how pregnancy incites or aggravates hypertension remains unsolved despite decades of intensive research. Various endocrine and metabolic mechanisms have been postulated to contribute to the pathogenesis of hypertension in pregnancy. Understanding the endocrine aspect of the possible pathophysiological mechanism might open new vistas in prediction, prevention and management of this condition.

While different generations of assays have played important role in elucidating causes of different endocrine disorders, radiological techniques are instrumental in localizing the pathology. This statement cannot be truer in any disease entity other than endocrine hypertension. This review makes an effort to highlight the role of different radiological modalities, especially ultrasonography, computed tomography and magnetic resonance imaging, in the evaluation of different causes of endocrine hypertension.

Objectives: The recent years have seen a surge in the prevalence of both diabetes and hypertension. Significant demographic variations reported on the prevalence patterns of diabetes and hypertension in India establish a clear need for a nation-wide surveillance study. The Screening India's Twin Epidemic (SITE) study aimed at collecting information on the prevalence of diagnosed and undiagnosed diabetes and hypertension cases in outpatient settings in major Indian states to better understand disease management, as well as to estimate the extent of underlying risk factors. Materials and Methods: During 2009-2010, SITE was conducted in eight states, in waves - one state at a time. It was planned to recruit about 2000 patients from 100 centers per wave. Each center enrolled the first 10 eligible patients (≥18 years of age, not pregnant, signed data release consent form, and ready to undergo screening tests) per day on two consecutive days. Patient demographics, medical history, and laboratory investigation results were collected and statistically interpreted. The protocol defined diabetes and hypertension as per the American Diabetes Association (ADA) and Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) recommendations, respectively. Results: After the first two pilot phases in Maharashtra and Delhi, the protocol was refined and the laboratory investigations were simplified to be further employed for all other states, namely, Tamil Nadu, West Bengal, Karnataka, Andhra Pradesh, Madhya Pradesh, and Gujarat. Conclusion: SITE's nation-wide approach will provide a real-world perspective on diabetes and hypertension and its contributing risk factors. Results from the study will raise awareness on the need for early diagnosis and management of these diseases to reduce complications.

Background: Elevated renin-angiotensin-aldosterone system (RAAS) activity is an important mechanism in the development of hypertension. Both obesity and 25-hydroxy vitamin D [25(OH)D] deficiency have been associated with hypertension and augmented renin-angiotensin system (RAS) activity. We tried to test the hypothesis that vitamin D deficiency and obesity are associated with increased RAS activity in Indian patients with hypertension. Materials and Methods: Fifty newly detected hypertensive patients were screened. Patients with secondary hypertension, chronic kidney disease, or coronary artery disease were excluded. Patients underwent measurement of vitamin D and plasma renin and plasma aldosterone concentrations. They were divided into three groups according to their baseline body mass index (BMI; normal <25 kg/m ² , overweight 25-29.9 kg/m ² and obese ≥30 kg/m ² ) and 25(OH)D levels (deficient <20 ng/ml, insufficient 20-29 ng/ml and optimal ≥30 ng/ml). Results: A total of 50 (male:female = 32:18) patients were included, with a mean age of 49.5 ± 7.8 years, mean BMI of 28.3 ± 3.4 kg/m ² and a mean 25(OH)D concentration of 18.5 ± 6.4 ng/ml. Mean systolic blood pressure (SBP) was 162.4 ± 20.2 mm Hg and mean diastolic blood pressure (DBP) was 100.2 ± 11.2 mm Hg. All the three blood pressure parameters [SBP, DBP and mean arterial pressure (MAP)] were significantly higher among individuals with lower 25(OH)D levels. The P values for trends in SBP, DBP and MAP were 0.009, 0.01 and 0.007, respectively. Though all the three blood pressure parameters (SBP, DBP and MAP) were higher among individuals with higher BMIs, they were not achieving statistical significance. Increasing trends in PRA and PAC were noticed with lower 25(OH)D and higher BMI levels. Conclusion: Vitamin D deficiency and obesity are associated with stimulation of RAAS activity. Vitamin D supplementation along with weight loss may be studied as a therapeutic strategy to reduce tissue RAS activity in individualswith Vitamin D deficiency and obesity.

Neurofibromatosis type 1 is the most common phakomatoses and is inherited in autosomal dominant fashion with complete penetrance. Secondary hypertension is common in these patients due to various causes including adrenal tumors. Pheochromocytoma is a rare catecholamine producing tumor seen in 0.5% to 5% of patients with neurofibromatosis. The combination of pheochromocytoma with neurofibromatosis is rarely reported in the literature. We recently encountered an elderly lady with this combination who successfully underwent adrenalectomy. We report the case for the uncommon occurrence and to highlight the relevant literature review about pheochromocytoma in neurofibromatosis.

Von Hippel-Lindau (VHL) disease includes a wide spectrum of highly vascular tumors like pheochromocytoma, cysts and adenomas of the pancreas and kidney, endolymphatic sac and renal cell carcinoma. Molecular analysis of the VHL gene is vital in these patients and their kindred. Neuroendocrine pancreatic tumors are rare and are known for their malignant and metastatic potential. We discuss an interesting case of a young lady who had a strong family history of central nervous system and spinal tumors. Our patient presented with recently detected severe hypertension. She was found to have elevated urinary normetanephrine levels; radiological imaging revealed bilateral pheochromocytomas with a pancreatic lesion. On genetic analysis, a variation, c.IVS 2 + 3 A > G, was found in the intronic region following exon 2 of the VHL gene. This variant appears novel. This patient underwent bilateral adrenalectomy (right total and left cortical sparing), distal pancreatectomy and splenectomy. Histology was diagnostic for pheochromocytoma with a neuroendocrine tumor of the pancreas. The postoperative period was uneventful. She was advised genetic screening of all her first-degree relatives.