Lack of Correlation Between Arterial and Venous β-Adrenergic Receptor Sensitivity

Abstract

Abstract The regulation of vascular β-adrenoceptor responses in humans has been studied in vivo in both arteries and veins. Because venous responses can be studied less invasively than arterial responses, they are an attractive substitute for the measurement of arterial responses, provided that venous responses are representative of responses in resistance arteries. However, although venous, particularly hand vein response, has been extensively studied, arterial and venous β-adrenergic sensitivities, in the same individuals, have not been compared. Measures of venous and arterial β-adrenergic sensitivities were compared in 10 healthy normotensive subjects. Forearm blood flow, after administration of increasing doses of isoproterenol into the brachial artery, was measured by strain-gauge plethysmography and was used for determination of arterial β-adrenoceptor sensitivity, expressed as the IP 500 (the dose of isoproterenol resulting in a fivefold [500%] increase in baseline forearm blood flow). Venous sensitivity to isoproterenol, expressed as the IP 15 (the dose of isoproterenol resulting in 15% venodilation), was measured in a dorsal hand vein using the linear variable differential transformer. Administration of isoproterenol into the hand vein and brachial artery resulted in venodilation and increased forearm blood flow, respectively. However, there was no correlation between the measures of venous (log IP 15 ) and arterial (log IP 500 ) measures of vascular β-adrenergic sensitivity ( r =−.12, P =.74). We conclude that since arterial and venous sensitivities to isoproterenol in healthy white men did not correlate, venous and arterial β-adrenergic responses are regulated differently and that studies examining vascular β-adrenoceptor sensitivity would most appropriately be performed in a vessel representative of the vascular bed of interest.