Increased Responsiveness of Veins to Adrenergic Stimulation in Experimental Hypertension

Bevan, J A; Bevan, Rosemary D.; Pegram, B.L.; Purdy, Ralph E.; Su, Che

doi:10.1159/000158017

Cited by 13 publications

(10 citation statements)

References 2 publications

(2 reference statements)

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“…Regarding the latter, it may be accelerated due to increased drug sensitivity related to various degrees of the augmented sympathetic nerve activity demonstrated in CHF [28][29][30] and HT. 6,26,31 This is because Japanese Circulation Journal Vol.62, August 1998 we have observed hemilateral Pv drop in subjcts with cerebral infarction or cervical injury after bilateral lidocaine administrations, and a rapid drop in Pv was definitely observed in one subject who also exhibited visual venospasm. 5 Concerning the dose dependency of the Pv response, the scattering of ∆Pv after both drug doses in group 2 does not support that idea.…”

Section: Discussionmentioning

confidence: 80%

Venous Response After Lidocaine Administration in Arm Veins

et al. 1998

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We previously reported that cubital venous pressure (Pv) tended to increase initially, but this was followed by a drop in a dose-dependent response after intravenous lidocaine administration in subjects with various diseases. In this study we examined whether Pv responses after small-dose intravenous lidocaine administrations are related to the stimulating effect of lidocaine on vascular smooth muscle (VSM). In 5 subjects free of cardiovascular disease, Pv increased slightly with decreased pulsations after a 10 mg dose (p<0.01) with no change in central venous pressure. In the cinephlebographic test performed on 2 healthy volunteers, Pv increased during recovery from proximal venoconstriction caused by an injection of contrast medium mixed with 10 mg lidocaine. In 9 subjects with cardiovascular disease, ∆Pv spread in the same directions (+ or -) after 5 and 10 mg drug administrations. In 6 of those tested with both drug doses, ∆Pv had positive means and no significant difference was observed. Thus, Pv responses after small-dose lidocaine administrations are consistent with neither the stimulating effect of lidocaine nor with a dose-dependent response. They could be attributed to the spasmolytic effect of lidocaine on the basal tone of VSM, which could be modulated by disease conditions. (Jpn Circ J 1998; 62: 576 -580)

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Section: Discussionmentioning

confidence: 80%

Venous Response After Lidocaine Administration in Arm Veins

et al. 1998

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“…Although the maximum response to norepinephrine was not significantly altered, the norepinephrine ED 50 was apparently reduced in hypertension (20); the reduction could be related to the magnitude of the arterial blood pressure in the arterial tree proximal to the ligature. An increased sensitivity of blood vessels in hypertension has been observed by many investigators in a number of experimental models (13-14, 24, 29).…”

Section: Discussionmentioning

confidence: 82%

“…The increased responsiveness of the arteries was associated mainly with an increase in the mass of vascular muscle in the vessel walls; in the veins, the alpha receptors became hypersensitive to lnorepinephrine. Preliminary results of the studies on the veins have been previously published (20).…”

mentioning

confidence: 99%

Analysis of changes in reactivity of rabbit arteries and veins two weeks after induction of hypertension by coarctation of the abdominal aorta.

Bevan¹,

Bevan²,

Chang³

et al. 1975

Circulation Research

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Vessel dimensions and characteristic responses to norepinephrine were measured in various arteries and veins of the rabbit made hypertensive by partial constriction of the upper abdominal aorta. The ear, radial, and basilar arteries taken from the circulation proximal to the ligature (the hypertensive arteries) were thickened in proportion to the rise in arterial blood pressure. The water, sodium, and potassium contents of these and all other vessels were not significantly changed in the hypertensive rabbits. The maximum response to norepinephrine in the ear artery, a representative vessel from the hypertensive part of the rabbit, was increased, whereas the sensitivity of this vessel to norepinephrine expressed as the ED 50 did not alter with changes in the arterial blood pressure. In contrast, the thickness and the maximum response to norepinephrine of the saphenous artery, representative of vessels distal to the ligature (normotensive vessels) and of the saphenous and cephalic veins were unaltered. The sensitivity as indicated by the norepinephrine ED 50 of the veins, but not of the saphenous artery, increased with a rise in carotid artery blood pressure. These results suggest that the increased responsiveness to norepinephrine of arteries proximal to the ligature is due to changes in muscle mass and that the increased responsiveness of the veins is due to increased sensitivity to norepinephrine.• The analysis of changes in responsiveness of blood vessels in hypertensive animal models has been the object of many investigations (1-14). A critical survey of these studies led us to define five experimental objectives, which served as the incentive for the present series of experiments. We wanted (1) to accurately determine the effect of hypertension on the responsiveness of vessels to norepinephrine in vitro using vessel rings; (2) to study a variety of vessels, including elastic and muscular arteries and veins, and (3) to separate local consequences of an increased intravascular pressure on the blood vessel wall from any generalized effects associated with the hypertensive state. We felt that (4) small early changes in the vessel wall should be observed if possible, since they are particularly relevant to the genesis of hypertension and that (5) control animal selection should minimize individual variation so that the small changes consequent to the hypertensive state could be recognized.The experimental model of hypertension which we chose to study was the rabbit with its abdominal aorta partially constricted between the celiac and anterior mesenteric arteries (15)(16)(17). In this preparation, after a few days the pressure in the arterial circulation proximal to the ligature becomes raised and that distal to the ligature returns to within the normal range. Although not all of our objectives were realized, many were satisfied by this approach. Existing techniques allowed measurements of vessel responsiveness to norepinephrine in both arteries and veins (18,19). A comparison of the changes in vessels tak...

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“…175 In rabbits with coarctation hypertension, 187 increased sensitivity of veins to nerve stimulation and exogenous norepinephrine has also been reported. In the one reported study of hypertensive patients, 188 responses of the forearm veins to catecholamines were normal.…”

Section: Venous Smooth Muscle Functionmentioning

confidence: 96%

“…187 Variability was so large, however, that a physiologically significant difference could not have been detected. This widely quoted study bears repeating with servo-null manometers and improved statistical design.…”

mentioning

confidence: 93%

Report of the Hypertension Task Force of the National Heart, Lung, and Blood Institute. Current research and recommendations from the Subgroup on Local Hemodynamics.

1980

Hypertension

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Increased Responsiveness of Veins to Adrenergic Stimulation in Experimental Hypertension

Cited by 13 publications

References 2 publications

Venous Response After Lidocaine Administration in Arm Veins

Venous Response After Lidocaine Administration in Arm Veins

Analysis of changes in reactivity of rabbit arteries and veins two weeks after induction of hypertension by coarctation of the abdominal aorta.

Report of the Hypertension Task Force of the National Heart, Lung, and Blood Institute. Current research and recommendations from the Subgroup on Local Hemodynamics.

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