Postsynaptic alpha 1- and alpha 2-adrenergic receptors in adrenergic control of capacitance vessel tone in vivo.

Elsner, Dietmar; Stewart, D.J.; Sommer, Olaf; Holtz, J.; Bassenge, E.

doi:10.1161/01.hyp.8.11.1003

Cited by 18 publications

(9 citation statements)

References 43 publications

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“…(Sigma Chemical, Munich, FRG) and by semilogarithmic extrapolation of arterial plasma concentration at injection time from several plasma samples, analyzed photometrically at 578 nm, obtained 10-40 minutes after the injection. [12][13][14][15][16][17][18] hours after the final diclofenac injection, these dogs were anesthetized and prepared for measurement of compliance under ganglionic and ,Badrenergic blockade as described for protocols 1-7. Compared with the effects of norepinephrine infusion in the same model, the COI in protocols 1 and 2 caused preferential venoconstriction.…”

Section: Measurementsmentioning

confidence: 99%

Preferential venoconstriction by cyclooxygenase inhibition in vivo without attenuation of nitroglycerin venodilation.

et al. 1988

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Because prostacyclin is a rather potent venodilator in vivo, we analyzed the effect of cyclooxygenase inhibition on venous tone in 14 anesthetized dogs during ganglionic and ,8-adrenergic blockade and atraumatic conditions. Effective vascular stiffness (a reciprocal of effective vascular compliance) as a variable of integrated venous tone was 0.30 + 0.01 mm Hg* kg/ml (n=35) and was augmented up to twofold by diclofenac (1, 3, and 10 mg/kg i.v.), ibuprofen (6 and 60 mg/kg), or indomethacin (5 mg/kg) parallel to augmentations in central venous pressure, while the rise in arterial pressure was less than half of the increase induced by equivenoconstrictor dosages of norepinephrine. After preconstriction by indomethacin or diclofenac, nitroglycerin (1.5 ,g/kg/min) lowered effective vascular stilfness (by 24+±2% or 23+± 5%, respectively), similarly as during preconstriction by norepinephrine (by 24 4%). Long-term cyclooxygenase inhibition (diclofenac 2 X 1 mg/kg/day for 4 days) did not modify arterial pressure, heart rate, or hematocrit levels in conscious dogs at rest, but it lowered plasma volume to 52.54±1.9 ml/kg (sham treatment: 59.1+±1.6 ml/kg, p

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Section: Measurementsmentioning

confidence: 99%

Preferential venoconstriction by cyclooxygenase inhibition in vivo without attenuation of nitroglycerin venodilation.

et al. 1988

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“…"-' 5 A recently published study by Segstro and Greenway 13 demonstrated that the hepatic volume of the cat, monitored plethysmographically, decreases in the presence of an a 2 -agonist. The finding by Eisner et al 20 that UK 14,304 decreases effective vascular compliance in the dog with ganglionic blockade also provides evidence for a direct hemodynamic effect of an a 2 -agonist on the venous circulation. Evidence for the decrease in vascular capacitance found in the present study was not seen in the canine studies by Zandberg et al 18 and by Woodman and Vatner.…”

Section: Discussionmentioning

confidence: 85%

“…18 Similarly, after ganglionic blockade and /3-adrenergic receptor and muscarinic blockade in conscious dogs, 19 B-HT 920 did not increase cardiac output. However, a recent study by Eisner et al 20 has shown in anesthetized, spontaneously breathing dogs with ganglionic blockade that effective vascular compliance was higher and central venous pressure lower than in conscious dogs without ganglionic blockade. The administration of the a 2 -agonist UK 14,304 lowered compliance and increased central venous pressure to levels found in conscious dogs.…”

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confidence: 95%

Direct effects of alpha 2-adrenergic receptor stimulation on intravascular systemic capacity in the dog.

1988

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SUMMARY The role of a r adrenergic receptor stimulation in the regulation of systemic vascular capacity and venous return, a major determinant of cardiac output, is not well understood. With the influence of the central nervous system isolated from the systemic circulation, the direct peripheral vascular effects of two specific, chemically distinct a 2 -adrenergk receptor agonists, UK 14,304 and B-HT 920, were investigated in 19 dogs on total cardiopulmonary bypass with constant arterial perfusion and central venous pressure. Five-minute intra-arterial infusions of UK 14,304 (200 /ig/min) resulted in increased arterial resistance (mean arterial pressure increased 18 ± 4 [SEM] mm Hg; p<0.01) and a decrease hi systemic vascular capacity (81 ± 20 ml; p<0.01). This decrease in systemic vascular capacity appears to result from vasoconstriction, since there was no decrease in transhepatic resistance to portal flow and no significant change in hepatic vein flow to suggest redistribution of arterial blood flow. Yohimbine abolished both the arterial and systemic capacity effects, whereas prazosin did not. Intra-arterial administration of B-HT 920 (200 Oglmin) in five dogs produced similar changes in arterial resistance and systemic capacity. These findings provide direct evidence for /^-adrenergic control, not only of arterial resistance but also of systemic vascular capacity, which in the intact nnlmnl would increase venous return to the heart. (Hypertension 11: 352-359, 1988) KEY WORDS • UK 14,304 • B-HT 920 • yohimbine • canine T HE importance of the regulation of systemic vascular capacity, which in turn determines venous return to the heart and thus cardiac output, has been a subject of recent investigation. l~* /3-Adrenergic receptor stimulation has been shown to decrease vascular capacity, 1 " 3 and acetylcholine infusion and parasympathetic nerve stimulation have been shown to increase vascular capacity. 4 The role of aadrenergic stimulation in the regulation of systemic vascular capacity is less well understood. Postsynaptic cr 2 -adrenergic receptors have been demonstrated in the

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“…However, previ ous studies (13,14) have shown that these changes were in dependent of EVS. (2) LNNA-induced increase in central venous pressure may also alter EVS.…”

Section: Discussionmentioning

confidence: 98%

Effect of N-Nitro-L-Arginine on Effective Vascular Stiffness in Dogs

Yamanaka

Itoh

Yukimura

et al. 1993

Japanese Journal of Pharmacology

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ABSTRACT-It has been reported that there is a continuous release of nitric oxide (NO) that contributes to the regulation of vascular tone in the arterial system. In contrast, the role of NO on vascular tone in the venous system is controversial. We examined the effect of IVY-nitro-L-arginine (LNNA), an NO synthase in hibitor, on venous tone in dogs. Venous tone was evaluated by effective vascular stiffness (EVS), which was calculated from the changes in central venous pressure recorded simultaneously with changes in blood volume. LNNA (10 mg/kg, i.v.) increased EVS from 0.21 ±0.04 to 0.30±0.03 mmHgl kg/ml as well as in creasing the systemic vascular resistance. N -Nitro-D-arginine had no effect on EVS. The LNNA-induced in crease in EVS was partly reversed by L-arginine, but not by D-arginine, indicating that the increase in EVS was attributable to a blockade of NO synthesis. Since the present study was conducted under ganglion blockade, nitroxidergic nerve terminals do not seem to be the source of NO in this case. These findings sug gest that NO (endothelium-derived relaxing factor) is constantly released in the venous system and con tributes to the regulation of total systemic venous tone.

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Postsynaptic alpha 1- and alpha 2-adrenergic receptors in adrenergic control of capacitance vessel tone in vivo.

Cited by 18 publications

References 43 publications

Preferential venoconstriction by cyclooxygenase inhibition in vivo without attenuation of nitroglycerin venodilation.

Preferential venoconstriction by cyclooxygenase inhibition in vivo without attenuation of nitroglycerin venodilation.

Direct effects of alpha 2-adrenergic receptor stimulation on intravascular systemic capacity in the dog.

Effect of N-Nitro-L-Arginine on Effective Vascular Stiffness in Dogs

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