Effect of beta-adrenergic blockade and inhibitors of angiotensin II and prostaglandins on renal autoregulation.

نویسندگان

  • R J Anderson
  • M S Taher
  • R E Cronin
  • K M McDonald
  • R W Schrier
چکیده

The role of the renin-angiotensin system and prostaglandins in renal autoregulation was investigated in dog kidneys in situ. Renal autoregulation during decreases in renal arterial pressure (RAP) was examined in animals pretreated with a competitive antagonist of angiotensin ii, [1-sarcosine, 8-glycine] angiotensin II, or one of two chemically dissimilar inhibitors of prostaglandin synthetase, indomethacin and meclofenamate. Because of recent evidence suggesting a role for an intrarenal beta receptor in regulating renin release, renal autoregulation was also examined in animals treated with the beta-adrenergic blocking agent propranolol. In all groups of animals constancy of glomerular filtration rate (GFR) and renal blood flow (RBF) was observed after substantial decreases in RAP to a range of 70-90 mmHg. These studies therefore do not provide evidence in support of a role for angiotensin II, prostaglandins, or an intrarenal beta receptor as mediators of the renal autoregulation of GFR or total RBF.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Renin-angiotensin system and unilateral ureteral obstruction

Unilateral ureteral obstruction (UUO) is a clinical scenario that leads to obstructive nephropathy. UUO alters the expression of many mediators in the ipsilateral kidney. Renin-angiotensin system (RAS) is involved in UUO. Angiotensin II (Ang II) and angiotensin 1-7 (Ang 1-7) as the main arms of RAS influence kidney function which may alter by UUO. Ang II via Ang II receptor subtypes I (AT1R) ...

متن کامل

The Mechanism of Preventive Effect of Captopril on Renal Ischemia Reperfusion Injury is Independent of ATP Dependent Potassium Channels

Background: Renal ischemia reperfusion (IR) injury has been a major source of concern during the past decades and angiotensin converting enzyme (ACE) inhibitors have been successfully used to prevent this injury. There have been some controversial reports about the involvement of KATP channels in the mechanism of action of ACE inhibitors. In this study, we examined the effect of KATP channel bl...

متن کامل

Causes and consequences of increased sympathetic activity in renal disease.

Much evidence indicates increased sympathetic nervous activity (SNA) in renal disease. Renal ischemia is probably a primary event leading to increased SNA. Increased SNA often occurs in association with hypertension. However, the deleterious effect of increased SNA on the diseased kidney is not only caused by hypertension. Another characteristic of renal disease is unbalanced nitric oxide (NO) ...

متن کامل

Attenuation of nephrotoxic acute renal failure in the dog with angiotensin-converting enzyme inhibitor (SQ-20,881).

Angiotensin-converting enzyme inhibitor was used in dogs with uranyl nitrate-induced acute renal failure to evaluate (1) a possible protective effect of angiotensin blockade and (2)the role of angiotensin II in the generation of renal failure in this model. Angiotensin-converting enzyme inhibitor treatment attenuated the fall in glomerular filtration rate and renal blood flow during the first 6...

متن کامل

ACE inhibition and cardiovascular mortality and morbidity in essential hypertension: the end of the search or a need for further investigations?

Scientific evidence currently available supports the concept that renin-angiotensin blockade with angiotensin converting enzyme inhibitors as a first-line treatment exhibits in arterial hypertension beneficial effects in the prevention of mortality and morbidity comparable to those achieved with diuretics and beta-blockers. In addition, the renin-angiotensin blockade has also proved to be benef...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:
  • The American journal of physiology

دوره 229 3  شماره 

صفحات  -

تاریخ انتشار 1975