Evidence for a renomedullary vasodepressor hormone

被引:22
作者
Thomas, CJ
Woods, RL
Evans, RG
Alcorn, D
Christy, IJ
Anderson, WP
机构
[1] UNIV MELBOURNE, DEPT ANAT, PARKVILLE, VIC 3052, AUSTRALIA
[2] UNIV MELBOURNE, DEPT CELL BIOL, PARKVILLE, VIC 3052, AUSTRALIA
[3] BAKER MED RES INST, PRAHRAN, VIC 3181, AUSTRALIA
关键词
blood pressure; hypertension; kidney; medullipin; renal blood flow; renal medulla;
D O I
10.1111/j.1440-1681.1996.tb01179.x
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
1. Recent physiological experiments have established that increasing the perfusion pressure of the kidney causes the release of a vasodepressor substance from the renal medulla. 2. The substance is not a platelet activating factor, a prostaglandin or nitric oxide and the vasodepressor response to increased renal perfusion pressure is not due simply to inhibition of renin release. 3. The mechanisms by which the renomedullary vasodepressor substance lowers arterial pressure remain to be determined. Sympathoinhibition may account for part of the response, but the hypotension still occurs in autonomic ganglion blocked animals. 4. The source of the substance appears to be the renomedullary interstitial cells, though the control of the production and release of the substance remain to be determined. 5. The substance may be a lipid but it is get to be fully isolated and identified. 6. The threshold for release of the substance appears to be close to normal resting arterial blood pressure. 7. Despite strong evidence that the renal medulla releases a vasodepressor hormone in response to increased renal perfusion pressure, much is still to be determined regarding the physiology of this hormone and its involvement in the aetiology of hypertension.
引用
收藏
页码:777 / 785
页数:9
相关论文
共 69 条
[1]  
Anderson WP, 1995, CLIN EXP PHARMACOL P, V22, pS426
[2]   N-OMEGA-NITRO-L-ARGININE INHIBITS THE HUMORAL RENOMEDULLARY VASODEPRESSOR RESPONSE IN A WISTAR ASSAY RAT, OTHERWISE INDUCED BY EXTRACORPOREAL HIGH-PRESSURE PERFUSION OF AN ISOLATED KIDNEY [J].
BERGSTROM, G ;
RUDENSTAM, J ;
FOLKOW, B ;
KARLSTROM, G ;
GOTHBERG, G .
ACTA PHYSIOLOGICA SCANDINAVICA, 1992, 146 (04) :527-528
[3]   RENAL AND HEMODYNAMIC-EFFECTS OF NITRIC-OXIDE BLOCKADE IN A WISTAR ASSAY RAT DURING HIGH-PRESSURE CROSS-CIRCULATION OF AN ISOLATED DENERVATED KIDNEY [J].
BERGSTROM, G ;
RUDENSTAM, J ;
CREUTZ, J ;
GOTHBERG, G ;
KARLSTROM, G .
ACTA PHYSIOLOGICA SCANDINAVICA, 1995, 154 (02) :241-252
[4]   CHEMICAL RENAL MEDULLECTOMY - EFFECT UPON REVERSAL OF 2-KIDNEY, ONE-CLIP HYPERTENSION IN THE RAT [J].
BING, RF ;
RUSSELL, GI ;
SWALES, JD ;
THURSTON, H ;
FLETCHER, A .
CLINICAL SCIENCE, 1981, 61 :S335-S338
[5]   CHEMICAL RENAL MEDULLECTOMY - EFFECT ON URINARY PROSTAGLANDIN-E2 AND PLASMA-RENIN IN RESPONSE TO VARIATIONS IN SODIUM-INTAKE AND IN RELATION TO BLOOD-PRESSURE [J].
BING, RF ;
RUSSELL, GI ;
THURSTON, H ;
SWALES, JD ;
GODFREY, N ;
LAZARUS, Y ;
JACKSON, J .
HYPERTENSION, 1983, 5 (06) :951-957
[6]  
BOHMAN SO, 1980, RENAL MEDULLA HYPERT, V7
[7]   QUANTITATIVE AND QUALITATIVE ANALYSES OF ISOLATED LIPID DROPLETS FROM INTERSTITIAL-CELLS IN RENAL PAPILLAE FROM VARIOUS SPECIES [J].
BOJESEN, I .
LIPIDS, 1974, 9 (11) :835-843
[8]  
Brooks B, 1994, Blood Press, V3, P407, DOI 10.3109/08037059409102295
[9]   EVIDENCE FOR A RENOMEDULLARY VASODEPRESSOR SYSTEM IN RABBITS AND DOGS [J].
CHRISTY, IJ ;
WOODS, RL ;
COURNEYA, CA ;
DENTON, KM ;
ANDERSON, WP .
HYPERTENSION, 1991, 18 (03) :325-333
[10]   MEDIATORS OF THE HYPOTENSIVE RESPONSE TO INCREASED RENAL PERFUSION IN RABBITS [J].
CHRISTY, IJ ;
WOODS, RL ;
ANDERSON, WP .
HYPERTENSION, 1993, 21 (02) :149-154