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.

No abstract

Control rats and rats with experimental renal hypertension due to unilateral stenosis of one renal artery received a standard diet (0.23% sodium) and a sodium-deficient diet (0.004% sodium), alternately, during which time blood pressure and plasma renin activity were determined. At the end of the experiment, renin content of the kidneys was measured. In normotensive control rats, the sodium-deficient diet did not affect blood pressure, but plasma renin activity and renin content of the kidneys increased. In rats with renal hypertension, restriction of sodium supply was followed by a fall in blood pressure to normotensive levels, provided that an intact contralateral kidney was present. Similarly, sodium-deficient diet prevented the development of hypertension if given immediately after placing the clip on one renal artery. Restriction of sodium supply provoked a marked increase in plasma renin activity, whereas renin content of the ischemic kidney was only slightly, but significantly, higher than in rats with normal sodium intake. Contrary to this, in unilaterally nephrectomized rats with renal hypertension, neither hypertension nor plasma renin activity or renin content of the kidneys was affected by sodium-deficient diet. In control rats with unilateral nephrectomy, plasma renin activity was only half that of intact rats, and restriction of sodium provoked no more than an increase up to normal values of intact rats. Sodium loss by the contralateral kidney may contribute to both the antihypertensive effect of a sodium-deficient diet and the increase in plasma renin activity.

No abstract

SUMMARY To examine tbe role of rasopressin (VP) in DOCA-salt hypertension, arterial pressure and renal vascular reactirity were studied in control Long-Erans (LE) rats and in Brattleboro rats homozygous for diabetes insipidus (DI rats). Vascular reactirity to norepinephrine, VP and angiotensin II was assessed in isolated kidneys perfused at constant flow. LE rats snowed an increase in arterial pressure (AP) which was significant at 2 weeks post DOCA and averaged 180 mm Hg at 4 weeks. DI rats lacking VP showed no rise in AP after DOCA; however, DI rats given VP and DOCA developed hypertension with a course and magnitude similar to that observed in LE rats. At 6 to 10 weeks post DOCA, renal vascular reactivity to all agents was increased in LE rats and DI rats replaced with VP. Nonnotensive DI rats lacking VP snowed depressed reactivity. Assessment of changes in reactirity at 3 days post DOCA showed that changes preceded tbe rise in AP. These data suggest that VP may play a primary role in the patbogenesis of DOCA hypertension and that its mechanism may involve an induction of increased vascular reactirity. T HERE has been increasing evidence that vasopressin may play a role in the development of DOCA-salt hypertension. Elevations in plasma levels 1 and urinary excretion* of vasopressin (VP) have been reported in DOCA-salt hypertensive rats. Furthermore, administration to these rats of VP antagonists* or a VP antiserum 1 produces an acute reduction in arterial pressure suggesting that the hypertension is maintained, in part, by a VP mechanism. It is also notable that Brattleboro rats homozygous for diabetes insipidus (DI rats), which totally lack VP and the ability to synthesize the hormone, fail to develop hypertension when treated with DOCAsalt.'-' The mechanism by which VP might participate in DOCA-salt hypertension is not understood. In earlier experiments, however, it was observed that renal vascular reactivity to norepinephrine (NE), VP, and angiotensin II (All) was increased in DOCA hypertensive rats not only in the chronic stage but in the prehypertensive stage, 4 suggesting that changes in vascular reactivity, per se, participate in the development of DOCA hypertension.The purposes of the present studies were to determine: 1) whether VP replacement in DI rats restores the hypertensive properties of DOCA-salt; and 2) to define the nature of changes in vascular reactivity in these rats after DOCA to determine whether restoration by VP of hypertension in VP-deficient rats might be associated with an induction of increased vascular reactivity. Methods Experimental AnimalsStudies were carried out on 12-week-old male Brattleboro rats homozygous for diabetes insipidus (DI rats) and Long Evans rats (LE rats) obtained from Blue Spruce Farms. At this age the average weight of the DI rats was 255 ± 9 g while that of the LE rats was 346 ± 7 g. Rats were housed individually in metabolic cages and fed a standard laboratory rat chow (Purina,