Peptides and Blood Vessels

Schmid, Phillip G.; Sharabi, Fouad M.; Phillips, M. Ian

doi:10.1002/cphy.cp020322

Cited by 5 publications

(4 citation statements)

References 202 publications

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“…20 In other vascular beds such as the mesentery, the vascular response to vasopressin varies with the vascular segment decreasing from venule to capillary to metarteriole to arteriole. 21 The mechanism responsible for these varying responses is not entirely clear but may involve different receptor populations. Presently, at least two distinct receptor populations for vasopressin have been identified.…”

Section: Mechanisms Of Differential Responses Of Coronary Microcirculmentioning

confidence: 99%

“…38 - 39 Previous studies in our laboratory indicate that the coronary microvasculature responds in a heterogeneous manner to neurally released or circulating norepinephrine after /3-adrenergic blockade. 40 Vasopressin also potentiates the effects of norepinephrine in rat mesentery 21 - 41 and can act centrally to alter sympathetic outflow. 21 In addition, vasopressin activates synthesis of prostaglandin E2.…”

Section: Mechanisms Of Differential Responses Of Coronary Microcirculmentioning

confidence: 99%

“…40 Vasopressin also potentiates the effects of norepinephrine in rat mesentery 21 - 41 and can act centrally to alter sympathetic outflow. 21 In addition, vasopressin activates synthesis of prostaglandin E2. 21 These indirect actions of serotonin and vasopressin could result in different vascular responses depending on the degree to which these secondary mechanisms are stimulated and the ability of a particular vessel size to respond to these stimuli.…”

Section: Mechanisms Of Differential Responses Of Coronary Microcirculmentioning

confidence: 99%

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Nonuniform vasomotor responses of the coronary microcirculation to serotonin and vasopressin.

Lamping

Kanatsuka

Eastham

et al. 1989

Circulation Research

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Large-conduit coronary arteries respond to vasoactive stimuli differently than smaller coronary arterioies, but the quantitative effects of many vasoactive stimuli at various levels of the microvasculature remain unknown. To determine the site of constriction or dilation to serotonin and vasopressin in the coronary microcirculation, we studied microvascular responses in the left ventricle of anesthetized cats (n =36). To compensate for motion due to contraction of the heart, the epicardium was visualized with stroboscopic epi-illumination controlled by a computer to flash once per cardiac cycle in mid-diastole, making the vessels appear stationary. Serotonin (16 /ig/kg/min) or vasopressin (0.5 units/min) was infused into the left atrium while maintaining aortic pressure constant with a snare on the descending aorta or inferior vena cava. Myocardial blood flow was measured with radioactive microspheres. During infusion of serotonin, aortic pressure and heart rate did not change, but myocardial perfusion increased 90±38% (mean±SEM) from a control value of 159±27 ml/min • 100 g. Arteries and arterioies larger than 90 /im constricted in response to serotonin (control 159±12 fim; percent change -18±3; range -41 to 10%) while arterioies less than 90 /tin dilated to serotonin (control 54±7 fim; percent change 22 ±9; range -10 to 62%). During infusion of vasopressin, aortic pressure and heart rate did not change, and myocardial perfusion decreased 16±7% (control, 147±18 ml/min • 100 g). In contrast to serotonin, infusion of vasopressin constricted arterioies less than 90 /un (control, 55±5 fim; percent change -16±3; range -27 to -2%) while arteries and arterioies larger than 90 /im did not respond or dilated modestly (control, 190 ±11 fim; percent change 4±2; range -29 to 43%). These responses to serotonin and vasopressin suggest that vasomotor regulatory mechanisms vary in different size arteries and arterioies in the coronary microcirculation, and the pivotal size at which differential changes occur is the 90 -/im level. (Circulation Research 1989;65:343-351) P revious studies of the coronary microcirculation have been hampered by the inability to visualize arterioies because of respiratory and cardiac-induced motion of the heart. Techniques that have been used to study segmental coronary vascular resistance include measurements of pressure gradients and measurements of large

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Section: Mechanisms Of Differential Responses Of Coronary Microcirculmentioning

confidence: 99%

Section: Mechanisms Of Differential Responses Of Coronary Microcirculmentioning

confidence: 99%

Section: Mechanisms Of Differential Responses Of Coronary Microcirculmentioning

confidence: 99%

See 1 more Smart Citation

Nonuniform vasomotor responses of the coronary microcirculation to serotonin and vasopressin.

Lamping

Kanatsuka

Eastham

et al. 1989

Circulation Research

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“…The baroreceptor system contains (among other peptides) SP in the carotid sinus and aortic arch regions, in the afferent nerves transmitting impulses from the Correspondence: Dr Jens H. Henriksen, Department of Clinical Physiology and Nuclear medicine, Hvidovre Hospital, DK-2650, Hvidovre, Denmark. baroreceptors to the brain (vagus and glossopharyngeal nerve), in the brain stem nuclei, and in neurons involved in cardiovascular control (Gillis et al, 1980;Pernow, 1984). The effects of central and peripheral administration of SP on the cardiovascular system have been studied in detail (von Euler & Pernow, 1977;Unger et al, 1980;Schmid et al, 1983), but little is known of the effect of acute changes in arterial blood-pressure on the level of plasma SP.…”

Section: Introductionmentioning

confidence: 99%

Arterial blood‐pressure change and endogenous circulating substance P in man

Henriksen

Kastrup

Muckadell

1985

Clinical Physiology

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Substance P (SP) is a powerful vasodilator and this peptide is today considered to be a chemical messenger. The potential effects on circulating SP of acute changes in arterial blood-pressure was investigated in nine subjects. An increase in arterial mean blood-pressure (+33%, P less than 0.001, n = 9) was obtained by infusion of angiotensin II and a decrease in pressure (-10%, P less than 0.005, n = 6) was obtained by ganglionic blockade. The concentration of SP in plasma, from supine subjects in the normotensive condition, ranged from 3 to 13 pmol/l (with a mean of 5.6 pmol/l). SP was thus within the reference interval: 3-16 pmol/l (n.s.). Plasma SP remained very constant in each subject during the changes in blood-pressure (mean variation in plasma concentration of SP was 0.97 (SD) pmol/l). The results show that acute changes in arterial blood-pressure do not result in any detectable change in plasma SP, this seems to indicate that endogenous circulating SP has no significant role in the vascular tonus controlled by the arterial baroreflex.

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Vasopressin causes endothelium-dependent relaxations of the canine basilar artery.

Katušić¹,

Shepherd

Vanhoutte

1984

Circulation Research

236

106

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The effect of synthetic 8-arginine vasopressin (vasopressin) was studied in isolated canine basilar, left circumflex coronary, and femoral arteries of the dog. Vascular rings with and without endothelium were suspended for isometric tension recording in physiological salt solution. The removal of the endothelium was confirmed by the absence of relaxations induced by either thrombin (basilar arteries) or acetylcholine (coronary and femoral arteries). In the basilar artery, vasopressin induced concentration-dependent inhibition of myogenic tone. In basilar and coronary arteries, the hormone caused concentration-dependent relaxations during contractions evoked by prostaglandin F2 alpha. In femoral arteries, vasopressin caused contraction. After removal of the endothelium, the inhibitory responses to vasopressin were abolished in basilar arteries and significantly reduced in left circumflex coronary arteries. The contractions of femoral arteries were not affected by endothelium removal. The V1-vasopressinergic antagonist d(CH2)5Tyr(Me)AVP prevented the inhibitory response to vasopressin, but did not alter endothelium-dependent relaxations of basilar arteries caused by adenosine diphosphate. These results demonstrate that the endothelial cells mediate relaxation induced by vasopressin via specific V1-vasopressinergic receptors.

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Peptides and Blood Vessels

Cited by 5 publications

References 202 publications

Nonuniform vasomotor responses of the coronary microcirculation to serotonin and vasopressin.

Nonuniform vasomotor responses of the coronary microcirculation to serotonin and vasopressin.

Arterial blood‐pressure change and endogenous circulating substance P in man

Vasopressin causes endothelium-dependent relaxations of the canine basilar artery.

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