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.
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.
We examined the distribution of common alleles of the ACE gene and measured circulating components of the renin-angiotensin system and urinary sodium excretion in 170 young Caucasian adults with contrasting genetic predisposition to high blood pressure.
Elevated plasma insulin levels may contribute to the development of hypertension through renal sodium reabsorption, the sympathetic nervous system, the transmembranous cation transport, the renin-angiotensin system, the cardiovascular reactivity, and the atrial natriuretic peptide.
Norepinephrine, renin activity, and total cholesterol blood concentrations were similar in normotensive patients with a positive family history of hypertension and in hypertensive patients with or without a family history.
Renin gene polymorphisms co-segregate with blood pressure in some genetic models, despite normal or low plasma renin and incorporation of an additional mouse renin gene construct into the rat genome produces severe hypertension despite suppression of renal renin.
Also tested in Utah studies, but not found to be DNA markers for hypertension, were the genetic loci for the structural genes for renin and angiotensin-converting enzyme, and the sodium antiport system.
In autosomal dominant polycystic kidney disease 1) the genetic localization of the defective gene that causes type 1 disease has been narrowed to 500 to 750 kb on chromosome 16; 2) cystogenesis has been associated with increased cell proliferation, continuing cyst secretion, and a defect in cell polarity; however, the mechanisms by which the genetic defects in autosomal dominant polycystic kidney disease translate into cyst formation are unknown; 3) activation of the renin system has been reported as an important potential cause of hypertension; and 4) factors that influence the progression to renal failure have been identified.
The syndrome of apparent mineralocorticoid excess (AME) is a form of low reninhypertension that is thought to be caused by congenital deficiency of 11 beta-hydroxysteroid dehydrogenase (11HSD) activity.
Approximately one half of the aldosterone-producing adenomas (APA) removed from patients with primary aldosteronism in the Hypertension Unit at Greenslopes Hospital belong to a subgroup in which aldosterone levels are responsive to the renin-angiotensin system (angiotensin-responsive APA; AII-R-APA), unlike classical APAs in which aldosterone is unresponsive (AII-U-APA).
Elevated and glucocorticoid-suppressible levels of the ZF 17-deoxysteroids--DOC and corticosterone--as well as their 18-hydroxylated products--18-OHDOC and 18-OHB (in addition to 19-nor-DOC)--are responsible for hypertension, hypokalemia, and renin and aldosterone suppression.
The angiotensin I-converting enzyme (ACE) is a key component of the renin-angiotensin system thought to be important in the pathogenesis of hypertension and cardiovascular disease.
We tested the hypothesis that overactivity of the renal and systemic renin-angiotensin system is important to the pathogenesis of hypertension in autosomal dominant polycystic kidney disease (ADPKD).
These data point to the importance of the renin-angiotensin system in both ischemic heart disease and hypertension, even without increased circulating levels of plasma renin.