Angiotensin II Receptor Modulation of Renal Vascular Resistance and Neurotransmission in Young and Adult Spontaneously Hypertensive Rats

2005 ◽  
Vol 28 (1) ◽  
pp. 20-26 ◽  
Author(s):  
Johannes Stegbauer ◽  
Oliver Vonend ◽  
Vitus Oberhauser ◽  
Lorenz Sellin ◽  
Lars Christian Rump
Keyword(s):  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Spontaneously Hypertensive Rats ◽  
Renal Vascular Resistance ◽  
Angiotensin Ii Receptor ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Receptor Modulation ◽  
Renal Vascular

Alterations in renal vascular resistance and reactivity in spontaneous hypertension of rats

1980 ◽  
Vol 238 (3) ◽  
pp. H287-H293 ◽  
Author(s):  
K. H. Berecek ◽  
U. Schwertschlag ◽  
F. Gross
Keyword(s):  
Vascular Resistance ◽  
Dose Response ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Response Curves ◽  
Renal Vasculature ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Dose Response Curves ◽  
Renal Vascular

Vascular resistance and reactivity were investigated in isolated, constant flow perfused kidneys of stroke-prone spontaneously hypertensive rats (SHRSP) and age- and sex-matched normotensive Wistar-Kyoto control rats (WKY rats). Stroke-prone spontaneously hypertensive rats were studied at 4 wk, 2 mo, and 4 mo of age representing different stages of development of hypertension. Resistance in maximally vasodilated vascular beds was greater and the pressure-flow relationship was significantly shifted to the left in kidneys of SHRSP as compared to WKY rats. Responses to norepinephrine, vasopressin, serotonin, and angiotensin II were enhanced in the renal vascular bed of SHRSP. Dose-response curves were shifted to the left, had steeper slopes, decreased thresholds, and increased maximal responses. With longer duration of hypertension, resistance increased, the slopes of the dose-response curves were steeper, and maximum responses greater. The higher resistance and enhanced reactivity in the renal vasculature of SHRSP, already demonstrable in the prehypertensive stage appear to be due to primary structural and functional alterations of the resistance vessels.

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