Hemodynamics of spontaneously hypertensive rats. I. Effects of pressure elevation

Ma, Pfeffer; Frohlich, E. D.

doi:10.1152/ajplegacy.1973.224.5.1066

Cited by 46 publications

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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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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 left ventricles were assayed for RNA, DNA, and hydroxyproline as previously described.' 5 A second group of SH and WKY rats was killed at age 80 days by decapitation without anesthesia and exsanguinated. Blood was collected in iced tubes containing ethylenediaminetetraacetic acid (EDTA) (1 mg/ml) for measurement of renin activity, or heparin (147 U/tube) for measurement of dopamine j8-hydroxylase activity.…”

Section: Methodsmentioning

confidence: 99%

Development of left ventricular hypertrophy in young spontaneously hypertensive rats after peripheral sympathectomy.

Cutilletta¹,

Erinoff²,

Heller³

et al. 1977

Circulation Research

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study of genetically determined hypertension and its effect on the cardiovascular system. 1 " 3 Our previous studies 4 and those of others 5>6 have demonstrated the presence of hemodynamic abnormalities accompanied by myocardial hypertrophy in the hypertensive adult rat. We also have been able to show that hypertension can be prevented by interventions in the immature rat which deplete central or peripheral catecholamines, or both. 7 -8 Administration of an antiserum to nerve growth factor to SH rats in the 1st week of life interferes with the development of sympa-

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“…The literature seems to consist of reports on the unaltered mechanical properties of isolated papillary muscles 13 and the increased intercapillary distance of superficial epicardial muscles. 19 In view of this and earlier data on some features of hemodynamic, 20 neurohumoral, 2 '-" and myocardial and coronary vascular histopathological 12 changes in this form of hypertension, we wanted to assess cardiac function and coronary hemodynamics in DOCA-salt hypertensive rats. Since we were interested in the concept of contractile'-5 -6 -8 and coronary flow (CF) I4~18 reserves, features important in comprehending the heart's behavior in the presence of hypertension, measurements were made not only under resting conditions but during inotropic and coronary vasodilator interventions.…”

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confidence: 99%

Cardiac contractile and coronary flow reserves in deoxycorticosterone acetate-salt hypertensive rats.

Yamamoto¹,

Tsuchiya²,

Saitō³

et al. 1985

Hypertension

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SUMMARY Cardiac contractility and coronary flow were compared in conscious rats with established deoxycorticosterone acetate-salt hypertension and in those with sham treatment. The hypertensive rats showed a 32% increase in left ventricular/body weight ratio at 9 weeks of treatment and 42% at 18 weeks of treatment. Resting peak rate of change of pressure (dp/dt) was unchanged at 9 weeks and increased at 18 weeks in hypertensive rats, while isoproterenol-stimulated maximal, propranololinduced minimal, and Ca 2+-stimulated maximal peak dp/dt were greater at 18 weeks. These data indicate the preservation of contractile function. At 18 weeks, the /3-adrenergic receptor-mediated contractile reserve, estimated from isoproterenol-stimulated maximal and resting peak dp/dt, was reduced but the propranolol-induced decrease in peak dp/dt was increased in hypertensive rats compared with sham-treated rats. Thus, at this stage, a greater portion of the total contractile capacity appeared to be mobilized with prolongation of hypertension and progression of left ventricular hypertrophy. No differences were observed in left ventricular and right ventricular coronary flow (microspheres) and left ventricular inner/outer flow ratio at rest and with dipyridamole-induced maximal coronary dilatation, at 9 and 18 weeks. There were no alterations in left or right ventricular coronary flow reserves, as estimated from resting and dipyridamole-induced values. The minimal coronary vascular resistance (normalized for gram of tissue) of both the left and right ventricles was increased at either stage, which suggests the occurrence of structural coronary vascular changes. Thus, basal coronary flow and a coronary flow reserve were uncompromised despite evidence of structural coronary vascular alterations in these hypertensive rats. (Hypertension 7: 569-577, 1985) KEY WORDS • left ventricular hypertrophy • minimal coronary vascular resistance peak rate of change of pressure (dp/dt) • radioactive microspheres • isoproterenol propranolol • dipyridamole S YSTEMIC hypertension often leads to alterations in cardiac performance associated with an increase in cardiac mass 1 "" and coronary circulation. '-l2 " 19 There is still considerable controversy regarding cardiac performance in the presence of hypertension, 1 ""-l3 most of which stems from the wide spectrum of cardiac function caused by variations in the duration, severity, and type of hypertension.Little is known of cardiac function and coronary hemodynamics in deoxycorticosterone acetate (DOCA)-salt hypertension. The literature seems to consist of reports on the unaltered mechanical properties of isolated papillary muscles 13 and the increased intercapillary distance of superficial epicardial muscles. 19 In view of this and earlier data on some features of hemodynamic, 20 neurohumoral, 2 '-" and myocardial and coronary vascular histopathological 12 changes in this form of hypertension, we wanted to assess cardiac function and coronary hemodynamics in DOCA-salt hypertensive rats. Since we ...

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Hemodynamics of spontaneously hypertensive rats. I. Effects of pressure elevation

Cited by 46 publications

References 0 publications

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

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

Development of left ventricular hypertrophy in young spontaneously hypertensive rats after peripheral sympathectomy.

Cardiac contractile and coronary flow reserves in deoxycorticosterone acetate-salt hypertensive rats.

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