Key result
Peripheral venous plasma from hypertensive patients enhanced tyramine-induced pressor responses by 67% (placebo) and 62% (thiazide) versus 33% with normotensive plasma (p < 0.05).
Why the study?
Does peripheral venous plasma from hypertensive patients alter vascular reactivity to angiotensin and norepinephrine in rats and dogs?
Does peripheral venous plasma from hypertensive patients alter vascular reactivity to angiotensin and norepinephrine in rats and dogs?
Absolute Event Rate: 67% vs 33%
p-value: p=< 0.05
Human peripheral venous plasma contains a substance that enhances tyramine-induced catecholamine release, but this substance likely does not play a role in essential hypertension.
Identifies circulating factor enhancing catecholamine release in animal models; leaves open its role in essential hypertension.
The effect of peripheral venous plasma (PVP) from normotensive sub;ects (Group A), and hypertensive patients who received placebo (Group B) or thiazide therapy (Group C) on vascular reactivity and resistance was evaluated in intact rats and dogs. Plasma electrolytes and serum levels of creatinine were normal in the three groups. Administration of 100 pl per kilogram of pVP from Groups A, B, or C did not affect the systemic pressure or the pressor responses to norepinephrine (NE) and angiotensin (A) in the anesthetized rat. The canine paw was perfused with autologous blood at constant flow. Intra‐arterial infusions of pVP (0.5 ml per minute) from Groups A, B, and C transiently reduced vascular resistance by 23 ± 11 %,35 ± 8%, and 8 ± 6% respectively. However, paw perfusion pressure returned to control values within 30 minutes. Pressor responses to NE were similar before and during infusion of pVP from each group. The pressor responses to tyramine (T) were enhanced by 33% during infusion of pVP from Group A and 67% (p < 0.05) and 62% (p < 0.05) during infusions of pVP from Groups Band C, respectively. Since PVP from Groups A, B, and C enhanced the pressor response to T but did not affect the response to NE, we conclude that a substance in human PVP enhances T‐induced catecholamine release. This substance probably does not play a role in essential hypertension.
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Greenberg et al. (1974) studied Hypertension. Peripheral venous plasma (PVP) from hypertensive patients vs. PVP from normotensive subjects was evaluated on Pressor responses to tyramine (p=< 0.05). Peripheral venous plasma from hypertensive patients enhanced tyramine-induced pressor responses by 67% (placebo) and 62% (thiazide) versus 33% with normotensive plasma (p < 0.05).
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