Hypertension and hyperpotassemia that were accompanied by normal plasma aldosterone and low renin levels and were responsive to chlorothiazide administration were found in a 29-year-old patient and two decades later in his 21-year-old son.
Further investigation of a family with normaldosteronemic hyperpotassemia and low-reninhypertension showed seven members from three generations, who ranged in age from 4 to 56 years, to be affected.
High blood pressure and elevated plasma renin activity have been normalized with a unilateral revascularization in the elder patient, and with the treatment of propranolol in the younger one.
In six additional patients with high renin levels induced by prior sodium depletion (10 mEq/day sodium diet), clonidine did not reduce blood pressure or renin, thus indicating that the suppressive action of this agent on renin pressor mechanisms occurs only in patients whose elevated renin levels are intrinsic to hypertension and unrelated to sodium depletion.
This review discusses a number of such techniques and their applicability to the study of diabetes and hypertension with the renin-angiotensin system as an example.
Essential hypertensive patients with an apparent hereditary component of hypertension can be characterized as the low-renin and Na-sensitive subgroup with intracellular Na+ accumulation.
The combined biochemical and genetic findings suggest that abnormalities of glucocorticoid metabolism and the renin-angiotensin system may help to explain genetic predisposition to high blood pressure.
Since the renin gene is a member of a conserved synteny group that in humans spans chromosome 1q21.3-32.3 and includes the gene for antithrombin III (AT3), we used linkage studies to examine the relationship between alleles of AT3 and hypertension in a family having 10 affected members.2.
This review discusses the impact of the availability of these clones in three clinically relevant areas--the role of the renin-angiotensin system in hypertension, the role of tissue renin-angiotensin systems, and the development of renin inhibitors.
These results suggest that the renal renin-angiotensin system plays a central role in the alterations in renal hemodynamics and sodium management associated with the development of hypertension in ADPKD.
1.In Gordon's syndrome (GS; a syndrome of hypertension and hyperkalaemia with normal glomerular filtration rate), excessive proximal sodium reabsorption leads to suppression of renin and aldosterone, hyperkalaemia and hyperchloraemic acidosis.2.
She presented all the features of the classical severe form of the disease: complete female phenotype; hypertension; hypokalemia; elevated levels of plasma progesterone, 11-deoxycorticosterone, corticosterone (B), and ACTH; and suppression of renin and aldosterone production.
The increased renin release, perhaps due to renal ischemia caused by cyst expansion, probably contributes to the early development of hypertension in polycystic kidney disease.
In subjects with a family history of hypertension, the renal vascular response to diltiazem was enhanced (p less than 0.01) despite similar values of plasma renin activity, angiotensin II concentration, and sodium excretion.
In a preliminary report, a study of the TaqI polymorphism of the human renin gene did not reveal a significant difference between hypertensive patients with a family history of hypertension and normotensive controls.
Although we found no genetic linkage in this set of study subjects, the characterization of the restriction fragment length polymorphisms for the renin gene may be useful in future studies of other selected pedigrees for the presence of one or more of these to be a genetic marker in hypertension.