Renal Vascular Resistance in Spontaneously Hypertensive Rats

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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Effect of Nifedipine on Renal Haemodynamics in an Animal Model of Cyclosporin a Nephrotoxicity

Clinical Science ◽

10.1042/cs0790259 ◽

1990 ◽

Vol 79 (3) ◽

pp. 259-266 ◽

Cited By ~ 14

Author(s):

P. G. McNally ◽

F. Baker ◽

N. Mistry ◽

J. Walls ◽

J. Feehally

Keyword(s):

Cyclosporin A ◽

Vascular Resistance ◽

Filtration Rate ◽

Spontaneously Hypertensive Rat ◽

Renal Plasma Flow ◽

Renal Haemodynamics ◽

Renal Vascular Resistance ◽

Hypertensive Rats ◽

Spontaneously Hypertensive ◽

Renal Vascular

1. This study investigates the effect of nifedipine on cyclosporin A nephrotoxicity in the spontaneously hypertensive rat. 2. Cyclosporin A, administered daily by subcutaneous injection at 25 mg/kg body weight for 14 days, induced a significant reduction in glomerular filtration rate (35.3%) and effective renal plasma flow (45.0%), and an increase in renal vascular resistance (219%). Using this regimen, tubular, glomerular or vascular morphological damage was not evident on light microscopy. 3. The administration of nifedipine simultaneously with cyclosporin A from day 1 prevented the characteristic decline in renal function and increase in renal vascular resistance. However, the administration of nifedipine to spontaneously hypertensive rats previously exposed to cyclosporin A for 7 days failed to improve renal haemodynamics. 4. This study suggests that the beneficial effect conferred by nifedipine on cyclosporin A nephrotoxicity is present only when treatment is initiated simultaneously with cyclosporin A.

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Segmental renal vascular resistance in the spontaneously hypertensive rat

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1982.242.6.h961 ◽

1982 ◽

Vol 242 (6) ◽

pp. H961-H966 ◽

Cited By ~ 2

Author(s):

C. H. Hsu ◽

J. H. Slavicek ◽

T. W. Kurtz

Keyword(s):

Vascular Resistance ◽

Spontaneously Hypertensive Rat ◽

Renal Vascular Resistance ◽

Hypertensive Rats ◽

Mean Values ◽

Spontaneously Hypertensive ◽

Microsphere Method ◽

Wistar Kyoto ◽

Renal Vascular ◽

Arteriolar Diameter

Renal hemodynamics were studied during different stages of development of hypertension in unanesthetized spontaneously hypertensive rats (SHR). In SHR at 4 wks of age mean arterial pressure (MAP) was higher than in age-matched Wistar Kyoto rats (WKY); however, renal blood flow (RBF) and renal vascular resistance (RVR) were not different between these two groups. Mean values of RVR and MAP in 8- and 12-wk-old SHR were significantly greater than those of age-matched WKY. Both RBF of 8- and 12-wk-old SHR were significantly lower than the corresponding values of WKY. Afferent arteriolar diameter (AAD) was measured with a microsphere method. AAD was not different between 4-wk-old SHR and WKY; however, the AAD of 8-wk-old (16.3 +/- 0.23 micrometers, n = 5) and 12-wk-old (17.4 +/- 0.48, n = 5) SHR were significantly smaller than those of respective control WKY (17.3 +/- 0.34, n = 4, P less than 0.05; 19.3 +/- 0.12, n = 5, P less than 0.01). Calculated preglomerular (Rpre) and postglomerular resistances (Rpost) of 12-wk-old SHR were increased 96 and 129% when compared with respective segmental resistances of the control WKY. The decrease in AAD of 12-wk-old SHR was sufficient to account for a 33% increase in Rpre. After the rats were treated with hydralazine (0.5 mg/kg iv), MAP, RBF, and RVR of SHR were not different from the control WKY values. Rpre and Rpost of SHR were substantially decreased; however, vasodilation occurred at vessels proximal and distal to the afferent arteriole because AAD was not altered. Our results indicate that increased RVR in SHR involves increases in Rpre and Rpost.

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