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.

Enhancement of alpha- and beta-adrenoceptor responses by elevations in vascular tone in pulmonary circulation

1986 ◽  
Vol 250 (6) ◽  
pp. H1109-H1116 ◽  
Author(s):  
A. L. Hyman ◽  
P. J. Kadowitz
Keyword(s):  
Vascular Tone ◽  
Beta Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Vascular Bed ◽  
Pressor Responses ◽  
Steady Level ◽  
Adrenoceptor Agonists ◽  
Beta 2 ◽  
Resting Tone ◽  
Pulmonary Vascular Bed

The influence of increases in vascular tone on responses to selective alpha 1- and alpha 2-adrenoceptor agonists, norepinephrine, epinephrine, and isoproterenol was investigated in the feline pulmonary vascular bed. Under resting tone conditions with constant pulmonary blood flow and left atrial pressure, intralobar injections of the alpha 1-adrenoceptor agonists, phenylephrine and methoxamine, and the alpha 2-adrenoceptor agonists, UK 14304 and B-HT 933, increased lobar arterial pressure. When pulmonary vascular resistance was raised to a high steady level, vasoconstrictor responses to the alpha 2-adrenoceptor agonists were markedly increased, responses to methoxamine were increased to a lesser extent, and pressor responses to phenylephrine and epinephrine were reversed. These vasodilator responses to phenylephrine and epinephrine at elevated vascular tone were blocked by propranolol. Moreover, after beta-adrenoceptor blockade, vasoconstrictor responses to phenylephrine, epinephrine, and norepinephrine were also greater at elevated tone than at resting tone. Vasodilator responses to the beta-adrenoceptor stimulant, isoproterenol, were enhanced at higher levels of vasoconstrictor tone and were blocked by propranolol and by albuterol, a selective beta 2-adrenoceptor antagonist. The enhanced vasoconstrictor responses to the alpha 2-adrenoceptor agonists were selectively blocked by yohimbine, whereas the enhanced responses to the alpha 1-adrenoceptor agonists and, for the most part, the vasoconstrictor responses to norepinephrine and epinephrine, were blocked by prazosin. The present data support the hypothesis that postjunctional alpha 1- and alpha 2-adrenoceptors mediating vasoconstriction and beta 2-adrenoceptors mediating vasodilation are present in the feline pulmonary vascular bed.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of stimulation of nucleus raphe dorsalis on carotid blood flow. II. The cat

1985 ◽  
Vol 248 (2) ◽  
pp. R263-R269 ◽  
Author(s):  
P. J. Goadsby ◽  
R. D. Piper ◽  
G. A. Lambert ◽  
J. W. Lance
Keyword(s):  
Intravenous Administration ◽  
Spinal Cord Section ◽  
Homocysteic Acid ◽  
Alpha Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Blocker ◽  
Raphe Dorsalis ◽  
Constrictor Response ◽  
The Brain ◽  
Stimulation Of

The dorsal raphe nucleus (DRN) and surrounding midbrain of 74 cats were stimulated both electrically and chemically, and carotid flows were measured with electromagnetic flow probes. Stimulation of the DRN caused a frequency-dependent decrease in common carotid vascular resistance, which was abolished by bilateral section of the facial nerve intracranially. Injection of DL-homocysteic acid into the DRN reproduced the effect of electrical stimulation, indicating that the responses arose from excitation of cell bodies within the DRN, not from fibers of passage. The responses were mediated entirely within the brain stem since they remained intact after high spinal cord section. The vasodilator response was blocked by the intravenous administration of the nicotinic ganglion blocker hexamethonium but not by the alpha-adrenoceptor blocker phentolamine. The responses were unaffected by intravenous administration of methysergide but were markedly reduced after depletion of central serotonin by pretreatment with the serotonin depletor, p-chlorophenylalanine. A poststimulus constrictor response was mediated by release of catecholamines from the adrenal medulla and was blocked by the alpha-adrenoceptor antagonist phentolamine. No response involved supracollicular mechanisms since they persisted after decerebration.

Alpha-1 Adrenoceptor Agonists Generate a “Fast” NMDA Receptor-Independent Motor Rhythm in the Neonatal Rat Spinal Cord

2004 ◽  
Vol 92 (2) ◽  
pp. 997-1010 ◽  
Author(s):  
H. Gabbay ◽  
A. Lev-Tov
Keyword(s):  
Nmda Receptor ◽  
Input Resistance ◽  
Nmda Receptor Antagonist ◽  
Neonatal Rat ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Blocker ◽  
Adrenoceptor Agonists ◽  
Current Steps ◽  
Lumbar Spinal ◽  
Fast Rhythm

Noradrenaline, a potent activator of rhythmogenic networks in adult mammals has not been reported to produce functional rhythmic patterns in isolated spinal cords of newborn rats. We now show that a “fast” (cycle time: 1–4 s) transient rhythm was induced in sacrococcygeal (SC) and rostral-lumbar spinal segments of the neonatal rat by bath-applied noradrenaline. The fast rhythm was blocked by 1 μM of the α1-adrenoceptor antagonist prazosin but not by 1–20 μM of the α2-adrenoceptor blocker yohimbine, it could be initiated and maintained by α1-adrenoceptor agonists, and it was accompanied by a slow nonlocomotor rhythm. Transection at the lumbosacral junction abolished the fast-thoracolumbar (TL) rhythm while the fast-SC and slow-TL rhythms were unaffected. The N-methyl-d-aspartate (NMDA) receptor antagonist 2-amino-5-phosphonopentanoic acid (AP5) abolished the slow- and did not interrupt the fast rhythm. Thus α1-adrenoceptor agonists induce an NMDA receptor-independent rhythm in the SC cord and modulate NMDA receptor-dependent rhythmicity in TL segments. Injection of current steps into S2 and flexor-dominated L2 motoneurons during the fast rhythm revealed a 20–30% decrease in input-resistance ( RN), coinciding with contralateral bursting. The RN of extensor-dominated L5 motoneurons did not vary with the fast rhythm. The rhythmic fluctuations of RN in L2 motoneurons were abolished, but the alternating left-right pattern of the fast rhythm was unchanged in midsagittally split TL cords. We suggest that the locomotor generators were not activated during the fast rhythm, that crossed-inhibitory pathways activated by SC projections controlled the rhythmic decrease in RN in L2 motoneurons, and that the alternating pattern of the split TL cord was maintained by excitatory SC projections.

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

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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