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Baroceptor Function in Chronic Renal Hypertension
The results of these experiments indicate that the carotid and aortic baroceptor mechanisms are reset to the hypertensive pressure levels of animals with chronic perinephritic hypertension and are, presumably, an important component in the mechanism of chronic renal hypertension.
Increased Cardiac Output as a Contributory Factor in Experimental Renal Hypertension in Dogs
Increased cardiac output probably has a contributory role in the development of renal hypertension, and absence of change in plasma volume and increase in mean circulatory pressure measured in a separate series of 7 dogs suggest that the initial increase in cardiac output preceding rise in pressure was due to enhanced venous return consequent to constriction of capacitance vessels.
Arterial Hypertension Elicited by Subpressor Amounts of Angiotensin
This indirect action of angiotensin to increase total peripheral resistance and arterial pressure by an action on the sympathetic nervous system, along with an upward resetting of the carotid sinus buffering mechanism, might logically account for the neural component of chronic renal hypertension.
Cardiovascular reactivity may be denned as the degree with which the heart and peripheral vascular bed respond to quantitated stimuli, whether the latter be drugs, reflex nervous activation, or nerve stimulation.
Renal Pressor System and Neurogenic Control of Arterial Pressure
By intensifying the effect of normal neurogenic vasomotor activity, this action of angiotensin, along with the upward shift of threshold and range of response of the carotid sinus buffer mechanism, might account to a major degree for the large neurogenic component of chronic renal hypertension.
Hemodynamic Characteristics of Chronic Experimental Neurogenic Hypertension in Unanesthetized Dogs
The hemodynamic changes accompanying experimental neurogenic hypertension due to sinoaortic denervation were measured in unanesthetized dogs for 3 weeks with chronically implanted arterial catheters and aortic flow transducers and the rises were consistently due to increase in peripheral resistance.
Cardiovascular Effects of Angiotensin Mediated by the Central Nervous System
• During recent years the nature of the considerable contribution of the sympathetic nervous system to renal hypertension has become somewhat more clear, due in part to the unexpected discoveries…
Sympathetic supraspinal control of venous membrane potential in spontaneous hypertension in vivo.
- W. Willems, D. Harder, S. Contney, J. Mccubbin, W. Stekiel
- Biology, MedicineThe American journal of physiology
- 1 September 1982
The data indicate that, in SHR, the relatively depolarized Em derives from altered alpha-adrenergic input, which is dependent on intact supraspinal pathways and appears to exert its depolarizing effect, at least in party, by interfering with the expression of endogenous, beta- adrenergic hyperpolarization.
Neural Stimulation of Release of Renin
It is concluded that neural stimuli are capable of causing release of renin in the absence of gross change in renal perfusion pressure or flow.
Inhibition of renin release by vasopressin and angiotensin.
Oxytocin did not affect renin release when infused in the same doses found to be effective for vasopressin, and the angiotensin analogues had no effects on arterial pressure, renal blood flow, or reninRelease.