peripheral vascular resistance

Following a major burn injury, heart rate and peripheral vascular resistance increase.

This may, however, worsen hypertension by increasing the peripheral vascular resistance.

It also increases peripheral vascular resistance, which in turn increases arterial blood pressure.

Several studies have shown a relationship between sodium sensitivity and the increase of circulating fluid volume or peripheral vascular resistance.

Vasopressin increases peripheral vascular resistance and thus increases arterial blood pressure.

One question is whether the increased peripheral vascular resistance may reduce cardiac output or rupture existing clots.

This decrease in peripheral vascular resistance is normally compensated for by an increase in the cardiac output.

Peripheral vascular resistance falls during the infusion of 1-8 mg etilefrine but begins to rise at higher dosage.

The method to assess sodium sensitivity includes the measurement of circulating fluid volume and peripheral vascular resistance.

This is in addition to increases in blood pressure, heart rate and peripheral vascular resistance associated with nicotine which may lead to recurrent angina attacks.

Additionally, by other mechanisms, HCTZ is believed to lower peripheral vascular resistance.

Pathogenic concepts currently believe that subtle changes to this microenvironment have pronounced effects on arterial tone and can severely alter peripheral vascular resistance.

The primary effect of this inhibition is relaxed vascular smooth muscle tone (vasodilation), which decreases peripheral vascular resistance, leading to decreased blood pressure.

At lower levels of circulating epinephrine, β-adrenoreceptor stimulation dominates, producing vasodilation followed by decrease of peripheral vascular resistance.

Nebivolol lowers blood pressure (BP) by reducing peripheral vascular resistance, and significantly increases stroke volume with preservation of cardiac output.

Increased sympathetic tone leads to increased peripheral vascular resistance and increased heart rate and contractility of the heart muscle.

Labetalol acts by blocking alpha and beta adrenergic receptors, resulting in decreased peripheral vascular resistance without significant alteration of heart rate or cardiac output.

This causes them to relax (vasodilation) resulting in a sudden decrease in blood pressure (secondary to a decrease in peripheral vascular resistance).

The drug induces vasoconstriction of skin and splanchnic blood vessels, thereby increasing peripheral vascular resistance and raising mean arterial blood pressure.

Clonidine treats high blood pressure by stimulating α receptors in the brain, which decreases cardiac output and peripheral vascular resistance, lowering blood pressure.

In addition AH-1058 has been shown to decrease systolic blood pressure while minimally affecting total peripheral vascular resistance and leaving diastolic blood pressure unaffected.

This reduces the volume of the blood, decreasing blood return to the heart and thus cardiac output and, by other mechanisms, is believed to lower peripheral vascular resistance.

For this purpose, magnesium may act as a vasodilator, with actions in the peripheral vasculature or the cerebrovasculature, to decrease peripheral vascular resistance or relieve vasoconstriction.

This improvement in performance of the ventricles is likely to result from a direct stimulation of the depressed myocardium as well as a decrease in peripheral vascular resistance.

Amlodipine is a peripheral arterial vasodilator that acts directly on vascular smooth muscle to cause a reduction in peripheral vascular resistance and reduction in blood pressure.