Contribution of cardiac output and peripheral resistance to experimental renal hypertension

Ferrario, C M

doi:10.1152/ajplegacy.1974.226.3.711

Cited by 59 publications

(12 citation statements)

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“…These observations have been confirmed and amplified in a variety of disparate types of experimental hypertension. Thus, whether a clip is placed around the renal artery of a rat or dog (Ledingham & Pelling, 1967;Ferrario, 1974), whether the animal is salt-loaded after removal of part of the renal mass (Coleman & Guyton, 1969), whether the kidney is encased in a perinephric hull (Ferrario, Page & McCubbin, 1970), or whether the animal is genetically sodium-sensitive (Tobian, Ganguli & Dahl, 1974) or spontaneously hypertensive (Pfeffer & Frohlich, 1973a), the evidence corroborates the observations first made in man (Eich el al., 1962) that the hypertension in its earliest stages is associated with a faster heart rate, higher cardiac output and increased myocardial contractility.…”

Section: Introductionmentioning

confidence: 99%

Adrenergic Mechanisms in Human Hypertension and in Spontaneously Hypertensive Rats

Frohlich

Pfeffer

1974

Clinical Science

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1. The role of adrenergic neuronal mechanisms in the development of early hypertension in man and the spontaneously hypertensive rat has been explored.2. In both, a hyperkinetic circulatory state is associated with reduced parasympathetic and increased adrenergic cardiac influences.3. Spontaneously hypertensive and normotensive control rats were treated with propranolol from conception until 12 weeks. Although heart rate and output remained reduced, there was no difference in growth or elaboration of pressure with respect to their untreated controls.4. After another series of spontaneously hypertensive and control rats received cardiac autonomic blockade (atropine and timolol), they sequentially received alpha-adrenergic blockade (phenoxybenzamine), ganglionic blockade (trimethaphan) and smooth-muscle vasodilatation (hydralazine). These studies revealed only a small pressure differential between the two groups before hydralazine and still less thereafter; unlike the control rats, pressure in spontaneously hypertensive rats fell markedly after ganglionic blockade as a result of reduced output, indicating greater adrenergic control mediated through venoconstriction. 5. These findings indicate: increased cardiovascular adrenergic control in young spontaneously hypertensive rats, the hyperkinetic circulation merely reflecting one aspect of increased total cardiovascular input. Structural alterations seem to participate minimally.6. These experimental observations closely resemble findings in early hypertensive man, and it is suggested that altered total cardiovascular adrenergic input is responsible for the elaboration, development, and maintenance of essential hypertension in man.

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Section: Introductionmentioning

confidence: 99%

Adrenergic Mechanisms in Human Hypertension and in Spontaneously Hypertensive Rats

Frohlich

Pfeffer

1974

Clinical Science

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“…An externally adjustable clamp was placed around the left renal artery (Ferrario, Blumle, Nadzam & McCubbin, 1971) so as to reduce its lumen by about 50%. It was further tightened 2 weeks later to occlude the vessel completely.…”

Section: Generalmentioning

confidence: 99%

“…By modifying previously reported techniques we have developed a simple and effective method of producing two-kidney hypertension in conscious dogs. This technique has two main significant advantages over previous methods : first, it does not depend on achieving a 'proper' amount of renal artery stenosis since the initial constriction is meant to serve only as a stimulus for the development of collateral circulation ; secondly, complete occlusion of the artery can be carried out rather easily with the use of a clamp that can be adjusted from the outside (Ferrario et al, 1971).…”

Section: Salinementioning

confidence: 99%

“…These results are consistent with those already described in the one-kidney Goldblatt model of hypertension by Bumpus ef al. (1973), Sweet, Ferrario, Kosoglov & Bumpus (1974) and Ferrario, Bumpus, Masaki, Khosla & McCubbin (1976). The similarity of effects obtained with the angiotensin antagonist in both forms of experimental renal hypertension argues against the concept that they differ in their pathogenesis.…”

Section: Salinementioning

confidence: 99%

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The Course of Arterial Pressure and the Effect of Sarxd1-Thr8-Angiotensin II in a New Model of Two-Kidney Hypertension in Conscious Dogs

et al. 1977

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1. We describe a new method of producing two-kidney hypertension in dogs by a two-step procedure with complete occlusion of a renal artery 2 weeks after it was partially constricted. 2. Control mean arterial pressure (96 +/- 3 mmHg) of nine conscious, trained dogs rose to 107 +/- 3 mmHg 2 weeks after partial constriction of a renal artery, and it stabilized at a sustained hypertensive plateau (124 +/- 7 mmHg) 3 weeks after complete occlusion. 3. Intravenous infusion of an angiotensin II antagonist (Sar1-Thr8-angiotensin II) caused arterial pressure to fall during the acute but not the chronic phase of renal hypertension. In this latter phase plasma renin activity had returned to control values. 4. We conclude that the renin-angiotensin system appears not to be directly involved in the chronic phase of two-kidney hypertension in the dog.

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“…In established human and experimental renal hypertension, blood pressure elevation is associated with an increase in total peripheral resistance (Ledingham & Pelling, 1967; Coleman & Guyton, 1969; Bianchi, Tilde Tenconi & Lucca, 1970;Coleman, Bower, Langford & Guyton, 1970; Kim, Onesti, Schwartz, Chinitz & Swartz, 1972;Tarazi, Frohlich & Dustan, 1973;Ferrario, 1974).…”

Section: Introductionmentioning

confidence: 99%

The Haemodynamic Response to Salt and Water Loading in Patients with End-Stage Renal Disease and Anephric Man

et al. 1976

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1. Patients with end-stage renal disease and anephric patients underwent expansion and depletion of body fluids with salt and water. This resulted in four different sequential haemodynamic patterns: (i) no significant increase in blood pressure; (ii) increase in blood pressure associated with a rise in cardiac output and no effect on total peripheral resistance; (iii) increase in cardiac output followed by a rise in blood pressure and total peripheral resistance; (iv) increase in total peripheral resistance and blood pressure without significant changes in cardiac output. 2. It is concluded that an initial rise in cardiac output is not necessary to increase blood pressure in either anephric man or patients with end-stage renal disease.

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Contribution of cardiac output and peripheral resistance to experimental renal hypertension

Cited by 59 publications

References 0 publications

Adrenergic Mechanisms in Human Hypertension and in Spontaneously Hypertensive Rats

Adrenergic Mechanisms in Human Hypertension and in Spontaneously Hypertensive Rats

The Course of Arterial Pressure and the Effect of Sarxd1-Thr8-Angiotensin II in a New Model of Two-Kidney Hypertension in Conscious Dogs

The Haemodynamic Response to Salt and Water Loading in Patients with End-Stage Renal Disease and Anephric Man

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