Vasoconstrictor reactions in spontaneously hypertensive rats versus Wistar Kyoto can be increased or decreased depending on the conditions of perfusion.

The reactions of resistance vessels in SHR and WKY hindquarters were compared during saline or blood perfusion. During saline constant-flow perfusion at all initial pressures (80-200 mmHg) sympathetic vasoconstrictor effects were greater in SHR than those in WKY. During perfusion at constant and equal pressure vasoconstrictor responses were greater in SHR vs. WKY only at high pressure--200 mmHg. On the other hand, under constant pressure conditions at lower pressures (80 and 120 mmHg) sympathetic stimulation induced weaker responses in SHR than in WKY, which at, for example, 80 mmHg was the case at every frequency of sympathetic stimulation used (2-20 Hz). Also, the responses to exogenous noradrenaline and vasopressin occurred during perfusion at low (80 mmHg) and for both equal constant-pressure conditions lower in SHR than in WKY. Comparison of sympathetic effects in SHR and WKY during blood hindquarter perfusion revealed similar results. Also, when SHR and WKY responses were compared at their ordinary levels of constant-pressure, sympathetic vasoconstrictor effects in SHR were lower than those in WKY.

[Comparative analysis of the efficacy of sympathetic effects on resistive vessels in spontaneously hypertensive and normotensive rats undergoing perfusion at a constant flow rate and under constant pressure]. / Sravnitel'nyi analiz éffektivnosti simpaticheskikh vliianii na rezistivnye sosudy spontanno gipertenzivnykh i normotenzivnykh krys pri perfuzii s postoiannym raskhodom i pod postoiannym davleniem.

The authors analyse the efficacy of sympathetic constrictive effects under the conditions of alternative perfusion. A more intensive vasoconstrictive response in perfusion with a constant discharge was observed in spontaneously hypertensive rats as compared to normotensive ones, and in perfusion with a constant pressure the reverse correlation was noted.

[Effect of captopril on arterial pressure, systemic hemodynamics and renin activity in the blood plasma of rats with spontaneous hypertension]. / Vliianie kaptoprila na arterial'noe davlenie, sistemnuiu gemodinamiku i aktivnost' renina v plazme krovi krys so spontannoi gipertenziei.

An angiotensin-I-converting enzyme, captopril, was administered since birth onward to normotensive (NR) and spontaneously hypertensive rats (SHR). It produced a marked hypotensive effect in SHR only. Cardiac output and circulating blood volume were similar in intact and experimental animals, NR and SHR alike. Captopril considerably increased plasma renin activity in NR and SHR.

[Delayed development of hypertension and increased aortic relaxation in spontaneously hypertensive rats after neonatal sympathectomy]. / Zamedlenie razvitiia gipertenzii i uvelichenie relaksatsii aorty spontanno gipertenzivnykh krys posle neonatal'noi simpatéktomii.

The effect of neonatal sympathectomy on vasodilator responses to acetylcholine (ACh) and cAMP has been studied in aortic rings of spontaneously hypertensive rats (SHR) and normotensive animals. The relaxation of intact SHR aorta in response to ACh and cAMP was 20-35% lower than that of normotensive rats. Sympathectomy in normotensive rats did not affect the level of blood pressure and aorta reactivity to Ach. In SHR, sympathectomy caused a decrease in blood pressure, while relaxation in response to ACh and cAMP increased, as compared to intact SHR, but remained lower than in normotensive rats. The data obtained suggest that the decrease in arterial pressure of sympathectomized SHR is a result not only of the reduction in sympathetic effects but also of the increase in smooth muscle relaxation.

[Age and changes in hemodynamics in the neonatally desympathized rat]. / Vozrastnye izmeneniia gemodinamiki u neonatal'no desimpatizirovannykh krys.

The hemodynamics was measured under resting conditions in chemically sympathectomized (with guanethidine) and control rats at 2.5, 4.0 and 8.0 months of age. In sympathectomized rats, the cardiac output (CO) was 23, 36 and 53% higher than in control, resp., whereas total peripheral resistance (TPR100) was 22, 27 and 42% lower, resp. The increase in CO was the result of elevation in the stroke volume. In sympathectomized rats, the TPR100 did not significantly change with age in contrast with control rats, and at 1.5 months of age an elevation of vascular resistance at maximal vasodilatation was observed in perfused isolated preparations. This difference diminished with age and disappeared at 4 or 8 months of age. The increase in structurally based resistance of vessels of sympathectomized rats at 1.5 months of age seems to be caused by reduced density of small resistance vessels.

[Effect of adaptation to high altitude hypoxia on the development of structural changes in the resistance vessels of the spontaneously hypertensive rat]. / Vliianie adaptatsii k vysotnoi gipoksii na razvitie strukturnykh izmenenii rezistivnykh sosudov u krys so spontannoi gipertenziei.

Adaptation to high altitude hypoxia prevents the development of arterial hypertension only in young spontaneously hypertensive rats (SHR) in the pre-hypertension stage. Adult SHR exposed to high altitude hypoxia showed no hypotensive effect. Judging by the experiments with extremities perfusion, the prophylactic effect of high altitude hypoxia in young SHR is associated with an increased number of resistant vessels. The increased ratio of the thickness of the vessel wall to the vascular lumen, however, remains unchanged probably due to the genetically determined development of hypertrophy of vascular smooth muscles.

[Systemic hemodynamic changes during the development of DOCA-salt hypertension. The effect of neonatal sympathectomy]. / Izmenenie sistemnoi gemodinamiki v protsesse razvitiia DOKA-solevoi gipertenzii. Vliianie neonatal'noi simpatéktomii.

The elevation of the cardiac index was discovered at the initial stage of DOCA-salt hypertension in rats. The blood pressure rise at the stage of stable hypertension was caused by an increase in the total peripheral vascular resistance. Neonatal sympathectomy prevented the development of DOCA-salt hypertension and elevation of the cardiac index revealed in control sympathectomized rats.

[Effect of chemical sympathectomy on the development of DOCA-salt hypertension in rats]. / Vliianie khimicheskoi simpatéktomii na razvitie DOKA-solevoi gipertensii u krys.

Structurally based resistance and vascular reactivity of the posterior body to noradrenaline were studied in normotensive rats and rats with DOCA-salt hypertension. The hypertension was induced in rats with intact sympathetic nervous system and in rats subjected to neonatal sympathectomy with guanethidine. During the prehypertensive stage, vascular sensitivity of the smooth muscles to noradrenaline was enhanced, with structural lesions being observed only in steady hypertension. Elevation of arterial pressure was accompanied by an increased vascular response to the stimulation of the sympathetic nerves. Sympathectomy prevented arterial pressure elevation and structural alterations in the vessels.

[Effect of neonatal sympathectomy on systemic hemodynamics and myocardial contractility in spontaneously hypertensive rats]. / Vliianie neonatal'noi simpatéktomii na sistemnuiu gemodinamiku i sokratimost' miokarda u spontanno gipertenzivnykh krys.

6-Hydroxydopamine was injected into normotensive rats (NR) and spontaneously hypertensive rats (SHR) during three weeks after birth. Cardiac output, blood pressure and heart contractility were measured in NR and SHR aged ten weeks. Sympathectomized SHR did not develop arterial hypertension. In these rats, cardiac output and heart contractility were decreased, whereas in sympathectomized NR, blood pressure was unchanged and cardiac output was increased. Possible mechanisms of the hemodynamic data are discussed.

[Mechanisms of the increased resistance to blood flow in the spontaneously hypertensive rat]. / Mekhanizmy povysheniia soprotivleniia krovotoku u krys so spontannoi gipertenziei.

Limb perfusion in spontaneously hypertensive rats demonstrated increased vascular resistance at maximum vasodilatation which may be related to structural specifics: the development of smooth muscle hypertrophy in resistive vessels and, obviously, decreased total number of functioning arterioles. The obtained "perfusion pressure - noradrenaline dosage" curves provide further evidence to this effect. The shift to the left shown by these curves and their greater steepness in spontaneously hypertensive rats are due to increased vascular reactivity to pressor effects.