scholarly journals Mechanisms of increased responses of the aorta to .ALPHA.-adrenoceptor agonists in streptozotocin-induced diabetic rats.

1988 ◽  
Vol 11 (10) ◽  
pp. 707-713 ◽  
Author(s):  
Katsuo KAMATA ◽  
Noriyuki MIYATA ◽  
Yutaka KASUYA
Keyword(s):  
Diabetic Rats ◽  
Alpha Adrenoceptor ◽  
Alpha Adrenoceptor Agonists ◽  
Adrenoceptor Agonists

Vascular responses to agonists in rat mesenteric artery from diabetic rats

1987 ◽  
Vol 65 (7) ◽  
pp. 1484-1490 ◽  
Author(s):  
Devendra K. Agrawal ◽  
John H. McNeill
Keyword(s):  
Diabetic Rats ◽  
Isometric Tension ◽  
Mesenteric Arteries ◽  
Diabetic Rat ◽  
Prostaglandin E ◽  
Contractile Responses ◽  
Alpha Adrenoceptor ◽  
Diabetic Model ◽  
Rat Mesenteric Artery ◽  
Adrenoceptor Agonists

The effect of diabetes on vascular smooth muscle function was investigated in the muscular arteries from spontaneously and chemically induced diabetic rats. Isolated ring segments of superior mesenteric arteries from BB diabetic and streptozotocin (STZ)-diabetic rats (12 weeks after onset of diabetes) were used for isometric tension studies. Contractile responses to alpha-adrenoceptor agonists (norepinephrine, methoxamine, phenylephrine, B-HT 920, guanabenz, SKF 89748-A), serotonin, and K+ were significantly higher in STZ-diabetic rat arteries as compared with the controls. In spontaneously diabetic rat arteries only the contractile responses to the putatively selective alpha2-adrenoceptor agonists, K+ and prostaglandin E1, were significantly increased. pD2 values of the agonists in both groups of diabetic arteries were not significantly different from the respective controls. Nifedipine inhibited all contractile responses in a dose-dependent fashion. The responses to K+ and alpha2-adrenoceptor agonists were attenuated to a greater extent by nifedipine in both groups of diabetic blood vessels. The calcium channel activator, BAY K 8644, produced a twofold increase in force of contraction in streptozotocin-diabetic and spontaneously diabetic rat arteries as compared with the responses in their respective controls. These results suggest caution in extrapolating all the findings from the streptozotocin-induced diabetic model to the spontaneously diabetic model. However, increased activity of calcium channels in vascular muscle cells in both groups of diabetics may be responsible, at least in part, for the increased vascular contractility in diabetes mellitus.

Quantitative relationships between .alpha.-adrenergic activity and binding affinity of .alpha.-adrenoceptor agonists and antagonists

1984 ◽  
Vol 27 (4) ◽  
pp. 495-503 ◽  
Author(s):  
Pieter B. M. W. M. Timmermans ◽  
Adriaan De Jonge ◽  
Martin J. M. C. Thoolen ◽  
Bob Wilffert ◽  
Harry Batink ◽  
...  
Keyword(s):  
Binding Affinity ◽  
Alpha Adrenoceptor ◽  
Alpha Adrenoceptor Agonists ◽  
Adrenergic Activity ◽  
Adrenoceptor Agonists

Evidence for existence of postjunctional alpha 1- and alpha 2-adrenoceptors in cat pulmonary vascular bed

1985 ◽  
Vol 249 (4) ◽  
pp. H891-H898
Author(s):  
A. L. Hyman ◽  
P. J. Kadowitz
Keyword(s):  
Adrenergic Nerve ◽  
Alpha Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Vascular Bed ◽  
Alpha Adrenoceptor Agonists ◽  
Adrenoceptor Blocker ◽  
Adrenoceptor Agonists ◽  
Uk 14,304 ◽  
6 Hydroxydopamine ◽  
Pulmonary Vascular Bed

The subtypes of postjunctional alpha-adrenoceptors in the feline pulmonary vascular bed were studied using selective alpha-adrenoceptor agonists and antagonists. Under conditions of controlled pulmonary blood flow and constant left atrial pressure, intralobar injections of the alpha 1-adrenoceptor agonists, phenylephrine and methoxamine, and the alpha 2-adrenoceptor agonists, UK 14,304 and BHT 933, increased lobar arterial pressure in a dose-related manner. Prazosin, an alpha 1-adrenoceptor antagonist, reduced responses to phenylephrine and methoxamine to a greater extent than responses to UK 14,304 and BHT 933. Yohimbine, an alpha 2-adrenoceptor blocker, decreased responses to UK 14,304 and BHT 933 without altering responses to phenylephrine or methoxamine. The same pattern of blockade was observed in animals pretreated with 6-hydroxydopamine, an agent that destroys the integrity of adrenergic nerve terminals. However, in propranolol-treated animals, prazosin antagonized responses to phenylephrine and methoxamine without altering responses to UK 14,304 or BHT 933, and the selectivity of the blocking effects of yohimbine were preserved. Responses to intralobar injections of norepinephrine were markedly decreased by prazosin, whereas yohimbine had only a small effect. These data suggest the presence of both postjunctional alpha 1- and alpha 2-adrenoceptors mediating vasoconstriction in the pulmonary vascular bed. These results also indicate that the vasoconstrictor responses to injected norepinephrine in the cat pulmonary vascular bed are due mainly to activation of alpha 1-adrenoceptors.

scholarly journals Mediation of contraction in rat cauda epididymidis by alpha-adrenoceptors

Reproduction ◽  
2002 ◽  
pp. 887-892 ◽  
Author(s):  
G Chaturapanich ◽  
S Maythaarttaphong ◽  
V Verawatnapakul ◽  
C Pholpramool
Keyword(s):  
Pressure Transducer ◽  
Systemic Effects ◽  
Alpha Adrenoceptors ◽  
Alpha Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Alpha Adrenoceptor Agonists ◽  
Adrenoceptor Agonists ◽  
Cauda Epididymidis ◽  
Spontaneous Contractions

Subtypes of alpha-adrenoceptors responsible for contractions of the rat cauda epididymidis were studied in vivo by micropuncture using a servo-nulling pressure transducer system. Administration of both non-selective and selective alpha-adrenoceptor agonists in doses of 1-40 microg noradrenaline kg(-1) body weight (BW), 1-100 microg clonidine kg(-1) BW, or 100-800 mg methoxamine kg(-1) BW enhanced contractions of the proximal cauda epididymidis in a dose-response manner. The potency of the agonists were noradrenaline > or = clonidine>methoxamine. Pre-treatments with selective alpha(1)-adrenoceptor antagonist (prazosin) and alpha(2)-adrenoceptor antagonist (yohimbine) at the doses of 400 and 800 microg kg(-1) BW, respectively, had very little effect on spontaneous contractions, but effectively blocked the responses to the maximal doses of methoxamine and clonidine. The responses could not be explained by the systemic effects of agonists and antagonists. The results suggest that contraction of the proximal cauda epididymidis of rats is mediated by both alpha(1)- and alpha(2)-adrenoceptors. The latter appears to be more abundant.

Coronary vasoconstriction mediated by alpha 1- and alpha 2-adrenoceptors in conscious dogs

1987 ◽  
Vol 253 (2) ◽  
pp. H388-H393 ◽  
Author(s):  
O. L. Woodman ◽  
S. F. Vatner
Keyword(s):  
Conscious Dogs ◽  
Similar Degree ◽  
Coronary Resistance ◽  
Coronary Vasoconstriction ◽  
Beta Adrenoceptor ◽  
Alpha Adrenoceptor ◽  
Alpha Adrenoceptor Agonists ◽  
Vasoconstrictor Response ◽  
Adrenoceptor Agonist ◽  
Adrenoceptor Agonists

Coronary vasoconstriction was examined in response to the selective stimulation of alpha 1- and alpha 2-adrenoceptors in chronically instrumented conscious dogs. Norepinephrine (NE, 0.05 and 0.1 micrograms X kg-1 X min-1), a mixed alpha 1- to alpha 2-adrenoceptor agonist, phenylephrine (PE, 0.5 and 1.0 micrograms X kg-1 X min-1), a preferential alpha 1-adrenoceptor agonist, and B-HT 920 (1.0 micrograms X kg-1 X min-1), a preferential alpha 2-adrenoceptor agonist, were infused intravenously after ganglionic (hexamethonium, 30 mg/kg iv), beta-adrenoceptor (propranolol, 1.0 mg/kg iv), and muscarinic receptor (atropine methylbromide, 0.1 mg/kg iv) antagonism. Equipressor doses of the alpha-adrenoceptor agonists caused similar increases in calculated late diastolic coronary resistance (NE, 0.57 +/- 0.10 mmHg X ml-1 X min; PE, 0.61 +/- 0.13 mmHg X ml-1 X min; B-HT 920, 0.64 +/- 0.09 mmHg X ml-1 X min). Mechanically increasing aortic root pressure to levels similar to those observed in response to alpha-adrenoceptor stimulation did not increase coronary resistance. Preferential antagonism of alpha 1-adrenoceptors with prazosin (1 mg/kg iv) abolished the vasoconstrictor response to PE but had a lesser effect on the response to B-HT 920. Antagonism of alpha 2-adrenoceptors with rauwolscine (alpha-yohimbine, 0.1 mg/kg iv) abolished the vasoconstrictor response to B-HT 920 but had a lesser effect on the response to PE. The response to NE was reduced to a similar degree by either alpha 1- or alpha 2-adrenoceptor antagonism.(ABSTRACT TRUNCATED AT 250 WORDS)

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