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Lack of physical activity can contribute to essential hypertension by leading to higher stress levels, greater risk of obesity, and reduced cardiovascular function. Several epidemiological studies have demonstrated a link between low physical activity and higher BP, mainly through the contribution of increased body mass in less active persons. 3. Genetics and certain rare types of secondary hypertension. Disorder Mode of inheritance Genes Mutation and functional consequences Glucocorticoidresponsive aldosteronism Autosomal dominant CYP11b1 and CYP11b2 Ectopic expression of aldosterone synthase activity in adrenal fasciculata Apparent mineralocorticoid excess Autosomal recessive 11bHSD Loss-of-function mutation resulting in excess stimulation of the mineralocorticoid receptor; hypertension mediated by increased renal cortical collecting tubule ENaC activity Mutations in mineralocortocoid receptor Autosomal dominant NR3C2 S810L missense mutation in the ligandbinding domain converts receptor antagonists (such as progesterone) to agonists; pregnancy exacerbates hypertension Liddle’s syndrome Autosomal dominant SCNN1B De-novo missense mutation of the b-subunit of the EnaC SCNN1G Mutation in the g-subunit of the EnaC that deletes the cytoplasmic C terminus, resulting in excess sodium retention Pseudohypo­ aldosteronism type II Autosomal dominant WNK1 and WNK4 WNK serine-threonine kinase defects resulting in hyperkalemia and hypertension Mutations in peroximase proliferator-activated receptor-g Autosomal dominant PPARG Loss-of-function mutation resulting in insulin resistance, diabetes mellitus, and hypertension Syndrome of hypertension, hypercholesterolemia, and hypomagnesemia Mitochondrial Not yet Maternal inheritance of a homoplasmic inheritance indentified mutation causes a cytidine substitution in the mitochondrial tRNA EnaC, epithelial sodium channel; CYP11b1, cytochrome P450, subfamily 11B, polypeptide 1; CYP11b2, cytochrome P450, subfamily 11B, polypeptide 2; 11bHSD, hydroxysteroid 11-b dehydrogenase; NR3C2, mineralocorticoid (aldersterone receptor); SCNN1B, sodium channel non-voltage-gated 1b (epithelial); SCNN1G, sodium channel nonvoltage-gated 1g; WNK1, protein kinase; WNK4, protein kinase, lysine deficient; PPARG, peroxisome proliferator activated receptor-g.

Therefore, blockade of the RAAS with ACE inhibitors or ARBs has significant therapeutic implications. Inhibition of the RAAS with ACE inhibitors or ARBs not only reduces the BP in patients with hypertension, it also protects against TOD. A variety of ACE inhibitors and ARBs are available for the treatment of hypertension, CHF, diabetic nephropathy (DN), and other ‘high-risk’ patients. Although ACE inhibitors and ARBs can be differentiated on the basis of their pharmacological, pharmacokinetic, and metabolic effects, these additional properties generally do not aid the clinician in the selection of drugs for the treatment of hypertension.

Other causes of secondary hypertension Cushing’s disease is caused by overproduction of cortisol. At high concentrations, cortisol can exhibit strong mineralocorticoid signaling that leads to hypertension. Interestingly, the morbidity and mortality associated with Cushing’s disease is most often due to diastolic hypertension. Other types of endocrine deregulation, such as disorders of the thyroid, hyperparathyroidism, and acromegaly, are also associated with hypertension. There are numerous other disorders of signaling or hormone production that are associated with elevated BP.