The Hemodynamics of the Rat During Ontogenesis, with Special Reference to the Age Factor in the Development of Hypertension

Albrecht, I.; Vízek, M; Krecek, J

doi:10.1007/978-3-642-65441-1_26

Cited by 20 publications

(10 citation statements)

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“…Mean body wt of the six spontaneously hypertensive rats (SHRs) was 328±2 g. Cardiac output for these rats is similar to that reported by Albrecht et al 17 in SHRs with established hypertension using the dye dilution method.…”

Section: Discussionsupporting

confidence: 84%

Antihypertensive action of medullipin I given by mouth.

et al. 1991

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Perfusion of normal rat kidneys with 5% human albumin in a balanced salt solution bubbled with oxygen yielded medullipin I (Med I) in the renal venous effluent The presence of Med I in the renal venous effluent has been established by thin-layer chromatography, by the type of vasodepressor effect when injected intravenously as a bolus into the hypertensive rat, by inhibition of the vasodepressor effect of the renal venous effluent by Tween 20 and SKF 525A (proadifen, inhibitor of cytochrome P-450), and by removal of the liver from the circulation (a procedure that inhibits extracted Med I). Med I so derived lowered blood pressure of spontaneously hypertensive rats when injected into the stomach by an indwelling tube or when given by mouth. The lowering of blood pressure was attended by no change in cardiac output and no change in heart rate. Med I given by mouth to the spontaneously hypertensive rat is a vasodilator that suppresses sympathetic tone, acting in the same way as Med I extracted from renal papillae and given intravenously. Importantly, the antihypertensive action was demonstrated in the spontaneously hypertensive rat, a model of hypertension considered to mimic idiopathic or essential hypertension of humans. Med I is a promising therapeutic agent for hypertension. (Hypertension 1991;17:1092-1096)

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Section: Discussionsupporting

confidence: 84%

Antihypertensive action of medullipin I given by mouth.

et al. 1991

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“…The hemodynamics of sponatneous hypertensive rats were examined by using 8(1 Rb dilution method under pentobarbital anesthesia. 13 Although absolute values of organ blood flow showed an increase only in the thyroid, with decreases in skin and gastrointestinal tract in that study, the direct effect of the anesthetic agent should not be neglected.…”

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confidence: 58%

Regional distribution of blood flow during arterial hypertension produced by lesions of the nucleus tractus solitarii in rats.

Snyder¹,

Doba²,

Reis³

1978

Circulation Research

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SUMMARY Changes in the fractional distribution of cardiac output (FF), organ blood flow, and regional vascular resistance were measured by the isotope dilution technique of Sapirstein using 86 Rb as indicator in unanesthetized rats during acute arterial hypertension produced by bilateral lesions of the nucleus tractus solitarii (NTS). After NTS lesions, the FF was significantly reduced in skin, muscle, and colon, increased in ventricular myocardium, spleen, and adrenal glands, and was unchanged elsewhere. Because of a marked reduction in cardiac output (CO) during hypertension, the absolute organ blood flow (FF x CO) was reduced in lesioned rats to 30-40% of control in skin, muscle, and colon and between 60% and 75% of control in most of the remainder of the gastrointestinal tract and renal cortex; it was unchanged in myocardium and endocrine glands. Resistance was substantially increased (4-to 6-fold) in skin, muscle and colon but was only moderately increased (1.5-to 2.5-fold) in the remaining organs. The results indicate that, while NTS lesions will increase resistance in most vascular beds, the response is unequally distributed, influencing skin, muscle, and colon disproportionately to other tissues. Because of an interaction between a reduction in CO and little autoregulation, blood flow is reduced primarily in skin, muscle, and colon. The pattern of redistribution of CO was consistent with the interpretation that NTS hypertension results from interrupting baroreceptor reflexes centrally. The pattern of redistribution of blood flow in rats with NTS lesions differs from that produced by deoxycorticosterone acetate-salt and renal ischemia. IN RATS, bilateral lesions of the nucleus tractus solitarii (NTS) results in the rapid development of arterial hypertension.1 In this model, termed NTS hypertension, the rise of blood pressure is presumed to be due to increased vasoconstrictor discharge resulting from central deafferentation of arterial baroreceptors by destruction of their primary synapse within NTS. As a result, the total peripheral resistance is markedly increased, leading to ventricular overload, reduction in cardiac output, progressive heart failure, and death associated with pulmonary edema within 3-4 hours.1 ' 2In the present study, we measured the changes in regional blood flow and in vascular resistances after lesions of NTS. Our objective has been 2-fold. First, we sought to determine whether the increase in total peripheral resistance produced by the lesion could be attributed to changes in vascular resistances within specific vascular beds reflecting, in turn, a differential activation of sympathetic neurons. Second, NTS lesions abolish arterial baroreceptor reflexes, 3 -4 and arterial baroreceptor activity is not uniformly distributed to all vascular beds, since vasoconstrictor activity in skeletal muscle is under greater baroreceptor control than that in kidney, skin, or the gastrointestinal tract. "10 Evidence of appropriate changes in resistance and flows in vascular beds after NTS lesions ...

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“…It has been reported that cardiac output is not enhanced and may even be slightly depressed during the chronic established phase of this hypertensive state (22,23). Since arterial blood pressure is a function of both cardiac output and peripheral resistance, the hypertensive state must derive from elevated peripheral resistance in the spontaneously hypertensive rat.…”

Section: Discussionmentioning

confidence: 99%

Neurogenic and Humoral Factors Controlling Vascular Resistance in the Spontaneously Hypertensive Rat

Lais

Shaffer

Brody

1974

Circulation Research

105

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The mechanism of sustained hypertension in spontaneously hypertensive rats has not been elucidated. In the present investigation, vasoconstrictor responses to a variety of neurogenic and humoral interventions were studied in the perfused hindquarters of Okamoto spontaneously hypertensive rats and normotensive Wistar rats. In addition, central sympathetic electrical discharge was measured. Vasoconstrictor responses in the hindquarters to lumbar sympathetic nerve stimulation were unchanged or reduced in the spontaneously hypertensive rats, but the responses to intra-arterially administered norepinephrine and epinephrine were enhanced. Vascular responses to intra-arterially administered tyramine, angiotensin, and barium chloride were also greater in the spontaneously hypertensive rats. Vascular resistance was significantly higher in the spontaneously hypertensive rats, and this difference remained following bilateral lumbar sympathectomy. Despite elevated systemic blood pressure, integrated nerve activity at rest was not different in the spontaneously hypertensive rats. The inverse relationship between arterial blood pressure and sympathetic nerve discharge was not different between spontaneously hypertensive and control rats when pressure was either raised or lowered. Changes in efferent sympathetic discharge produced by activation of chemoreceptors (asphyxia) were somewhat less in the spontaneously hypertensive rats. The contribution of low-pressure baroreceptors (45° tilt) to activation of sympathetic vasomotor tone was not different in the spontaneously hypertensive rats despite a greater decline in systemic blood pressure during the procedure. These data demonstrate that established hypertension in the spontaneously hypertensive rat does not derive from either enhanced central adrenergic discharge or altered central integration of afferent information from peripheral sensory receptors but may result from humoral (e.g., increased reactivity to vasoconstrictors) or structural factors. KEY WORDSvascular reactivity adrenergic vasomotor tone catecholamines central vasomotor control baroreceptors sympathetic nervous system chemoreceptors sympathectomy• The spontaneously hypertensive rat was isolated as a pure inbred strain by Okamoto and Aoki (1). In these rats, the hypertensive state develops without provocation and is readily apparent soon after weaning age (2). The pathophysiology underlying the development and the maintenance of hypertension in the spontaneously hypertensive rat has not been elucidated. Of the many factors that could contribute to the maintenance of hypertensive state, only the renin-angiotensin pressor system seems to be excluded from participation (3, 4). Some investigators (5-7) have suggested that the hypertensive state is maintained by an increase in neurogenic vasoconstrictor influences which should theoretically be associated with 764an increase in the turnover of catecholamines (8). However, a growing body of reports indicates a decrease in catecholamine turnover in peripheral t...

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The Hemodynamics of the Rat During Ontogenesis, with Special Reference to the Age Factor in the Development of Hypertension

Cited by 20 publications

References 1 publication

Antihypertensive action of medullipin I given by mouth.

Antihypertensive action of medullipin I given by mouth.

Regional distribution of blood flow during arterial hypertension produced by lesions of the nucleus tractus solitarii in rats.

Neurogenic and Humoral Factors Controlling Vascular Resistance in the Spontaneously Hypertensive Rat

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