Page 1 of 2: gold blatt hypertention

nadu · Credits: 17500 My Scrapbook

Q. GOLD BLATT hypertention is due to :

1.renovascular cause

2.idiopathic

3.drug induced

4.adrenal medullary tumor

drpsg · Credits: 6198 My Scrapbook

hi i m not sure but heard some where it is renovascular ht
will confirm and let u know

shankardada · Credits: 1867 My Scrapbook

Increased blood pressure following obstruction of blood flow to one kidney.

ondinescurse · Credits: 124 My Scrapbook

abe renovascular hai(ganong)

ondinescurse · Credits: 124 My Scrapbook

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ondinescurse · Credits: 124 My Scrapbook

ondinescurse · Credits: 124 My Scrapbook

renovascular

anandkumar_m · Credits: 3338 My Scrapbook

NORMAL AND HIGH RENIN HYPERTENSION

A number of explanations have been offered for the “inappropriately normal” or high levels of renin, beyond the proportion expected in a normal gaussian distribution curve.

One of the more attractive is the concept of “nephron heterogeneity” described by Sealey et al., which assumes a mixture of normal and ischemic nephrons caused by afferent arteriolar narrowing.

Pathogenesis: Excess renin from the ischemic nephrons ----> raise the total blood renin level to varying degrees ----> cause normal or high renin hypertension.

This hypothesis is similar to that proposed by Goldblatt, who believed that “the primary cause of essential hypertension in man is intrarenal obliterative vascular disease, from any cause, usually arterial and arteriolar sclerosis, or any other condition which brings about the same disturbance of intrarenal hemodynamics.” When Goldblatt placed the clamp on the main renal arteries in canine studies, he was trying to explain the pathogenesis of primary (essential) hypertension rather than what he ended up explaining: the pathogenesis of renovascular hypertension.
MECHANISMS of Renovascular hypetension.

Since Goldblatt produced renovascular hypertension in the dog in 1934, the pathophysiology of this disease has been studied extensively. Confusion has arisen because of the use of one-kidney models, which are more appropriate to the study of renal parenchymal hypertension. The sequence of changes in the two-kidney (oneclip) model and in patients with renovascular hypertension almost certainly starts with the release of increased amounts of renin when sufficient ischemia is induced to diminish pulse pressure against the juxtaglomerular cells in the renal afferent arterioles. A reduction of renal perfusion pressure by 50 per cent leads to an immediate and persistent increase in renin secretion from the ischemic kidney, with suppression of secretion from the contralateral one. With time, renin levels fall (but not to the low levels expected based on the elevated blood pressure), accompanied by an expanded body fluid volume and increased cardiac output.

Nonetheless, his experimental concept is the basis for the more modern model of Sealey et al. The elevated renin from the ischemic population of nephrons, although diluted in the systemic circulation, provides the “normal” renin levels that are usual in patients with primary hypertension who would otherwise be expected to shut down renin secretion and in whom levels would be low. These diluted levels are still high enough to impair sodium excretion in the nonischemic hyperfiltering nephrons but are too low to support efferent tone in the ischemic nephrons, thereby reducing sodium excretion in them as well.

nadu · Credits: 17500 My Scrapbook

thanx anand !

thats a good stuff.

Guest · Credits: 78895 My Scrapbook My Reading List 262569 Books

thanks Anand..great explanation!

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