Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PHENTOLAMINE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 937 records · Page 52Linked to original sources
PubMed1999

Effect of local sympathetic blockade on forearm blood flow and glucose uptake during hypoglycemia.

During hypoglycemia, hepatic glucose production increases and peripheral glucose utilization decreases. Systemic beta-adrenergic blockade during hypoglycemia increases peripheral glucose utilization. To explore the local effects of increased alpha- and beta-adrenergic activity on skeletal muscle glucose utilization, we measured arterial and venous plasma glucose concentrations, forearm blood flow (FBF), and forearm glucose uptake (FGU) during a hyperinsulinemic (40 mU/m2/min) stepped-hypoglycemic clamp with intrabrachial artery infusion of saline, phentolamine, propranolol, or combined phentolamine and propranolol. A control study was also performed with a euglycemic clamp and intraarterial saline. During hypoglycemia with saline and phentolamine, there were significant increases in FBF (130% +/- 38% and 180% +/- 35%, respectively) and FGU (120% +/- 51% and 230% +/- 150%, respectively). During hypoglycemia with propranolol and phentolamine + propranolol, FBF remained constant. FGU during hypoglycemia with propranolol was not different versus hypoglycemia with saline. No differences were found in these studies for forearm lactate output (FLO) or venous free fatty acid concentrations. These results demonstrate that local, as opposed to systemic, blockade during hypoglycemia does not alter peripheral glucose utilization.

Adrenergic alpha-Antagonists↗
PubMed1998

Receptor mechanisms of bradykinin-mediated activation of prenodal lymphatic smooth muscle.

We have previously shown that several endogenous vasoactive agents constrict prenodal lymph vessels in the canine forelimb. In this study, we assessed the receptor mechanisms by which bradykinin activates lymphatic smooth muscle. Intralymphatic (i.l.) infusion of bradykinin at concentrations of 3.82 x 10(-6), 3.82 x 10(-5) and 3.82 x 10(-4) molar significantly increased lymphatic perfusion pressure. To determine the potential role of lymphatic alpha-receptors in this response, we infused bradykinin at a concentration of 3.82 x 10(-4) molar i.l. before and during intra-arterial (i.a.) phentolamine administration. Prior to phentolamine, bradykinin resulted in a doubling of the lymphatic perfusion pressure. Phentolamine alone had no effect on the resting lymphatic pressure, but significantly reduced forelimb arterial pressures. When the infusion of bradykinin was repeated during phentolamine administration, there was no significant change in the lymphatic perfusion pressure. To determine the subclass of alpha-adrenergic receptors involved in this response, we infused bradykinin and the alpha1-receptor agonist phenylephrine i.l. before and during administration of i.a. prazosin, a specific alpha1-receptor antagonist, i.a. Prior to prazosin, both phenylephrine and bradykinin significantly increased lymphatic perfusion pressure. During prazosin administration, neither phenylephrine nor bradykinin significantly altered the lymphatic perfusion pressure. These data indicate that bradykinin-mediated increases in prenodal lymphatic smooth muscle tone are mediated by lymphatic alpha1-adrenergic receptors.

Adrenergic alpha-Agonists↗
PubMed2000

Effects of purinergic and adrenergic antagonists in a rat model of painful peripheral neuropathy.

In previous studies, pain behaviors produced in the spinal nerve ligation rat model of neuropathic pain were partly reduced by surgical lumbar sympathectomy. However, systemic injection of phentolamine, an alpha-adrenoceptor blocker, was not effective in reducing pain behaviors, at least in the Sprague-Dawley strain of rats. This suggests that sympathectomy removes not only adrenoceptor function but also other factors that must contribute importantly to the generation of neuropathic pain behaviors. Since the purinergic substance adenosine 5'-triphosphate (ATP) is known to be co-released with norepinephrine (NE) from the sympathetic nerve terminals, we hypothesized that ATP might be involved in the sympathetic dependency of neuropathic pain. The present study tested this hypothesis by examining the effects of systemic injection of an adrenoceptor blocker (phentolamine), a purinoceptor blocker (suramin), and a combination of these two on behavioral signs of mechanical allodynia in the spinal nerve ligation model of neuropathic pain. The results of the present study showed two novel findings. First, the mechanical hypersensitivity (allodynia) resulting from the L5/6 spinal nerve ligation can be reduced either by sympathetic block accomplished by application of a local anesthetic or by surgical sympathectomy of the L2-L6 sympathetic ganglia. Second, suramin (at 100 mg/kg, i.p.) can reduce mechanical hypersensitivity in neuropathic rats when given in combination with 5 mg/kg of phentolamine. This effect was observed in a subset of neuropathic rats, and the drug responses were consistent in repeated treatments within the animal group. Neither phentolamine nor suramin changed the mechanical sensitivity of neuropathic rats when given alone. The data suggest that the purinergic substance ATP is co-released with NE from sympathetic nerve terminals and these two are together involved, at least in part, in the maintenance of the sympathetically dependent component of pain behaviors in some neuropathic rats.

Adrenergic alpha-Antagonists↗
PubMed1997

Peripheral alpha-adrenoreceptors are involved in the development of capsaicin induced ongoing and stimulus evoked pain in humans.

While the sympathetic nervous system seems to be involved in some pain states, the mechanisms linking the sensory and sympathetic nervous system are unclear. In this study the possible involvement of peripheral alpha-adrenoreceptors in the development of capsaicin induced ongoing pain and mechanical hypersensitivity was examined in humans. Intradermal capsaicin injections in the volar aspect of the arm gave rise to ongoing burning pain and dysesthesia as well as mechanical hypersensitivity. Ongoing pain and pain evoked by von Frey filament stimulation was rated on a numerical rating scale after intradermal capsaicin injection. The area of skin in which von Frey filament stimulation evoked pain was measured. A subcutaneous injection of phentolamine (alpha-adrenoreceptor antagonist) on one side and saline on the other side prior to the capsaicin injection was done to evaluate the role of the peripheral alpha-adrenoreceptors in development of capsaicin induced sensory symptoms and signs. Significantly less ongoing and evoked pain developed on the phentolamine injected side compared to the saline side, the latter in the area adjacent to the capsaicin injection (primary zone) and well outside the area of flare (secondary zone). The area in which pain could be evoked on the phentolamine injected side was restricted to the area of flare and was significantly smaller than on the saline injected side. Mechanical stimulation gave rise to aftersensation and radiation of pain on the saline injected side in all subjects but only in one case on the phentolamine injected side. Peripheral alpha-adrenoreceptors thus seem to be involved in functional changes of primary afferents which contribute to ongoing pain and mechanical stimulus evoked pain.

Adrenergic alpha-Antagonists↗
PubMed2004

[Comparison of the uterine reflex activity during artificial insemination and mating in the ewe].

AIM: To identify and to compare the reflex mechanisms involved in the activation of the uterine motility following artificial insemination (AI) and mating in the ewe. MATERIALS AND METHODS: The contractile activity of the uterus was monitored in presence and absence of adrenergic (phentolamine) and cholinergic (atropine) antagonists, using an implantable telemetric device equipped with a sensor catheter inserted into the uterine lumen, and connected to a radio-telemetric transmitter. RESULTS: During AI, a uterine contraction (UC) of short duration (<20 seconds) appeared in direct response to animal restraint, to the speculum introduction, then when the speculum was opened. Both the UC evoked by restraint of the ewe and insertion of the speculum were abolished in presence of phentolamine, while atropine inhibited the UC in response to opening of the speculum only. After AI, the uterine activity increased sharply and was all the more intense and extended with higher vaginal wall pressure. Phentolamine or atropine did not inhibit this motor response, whereas a similar pattern of uterine hyperactivity occurred following i.v. injection of oxytocin (100 and 200 mIU; Syntocinon). After mating, an increase in uterine activity was never observed. Only penis intromission evoked a UC of short duration (about 20 seconds), abolished in presence of phentolamine only. CONCLUSION: Artificial insemination in the ewe increases uterine motility, resulting from the reflex activation of adrenergic and cholinergic nerve fibres of the autonomic nervous system, following by a reflex release of oxytocin from the pituitary gland (also called "Ferguson reflex"). This secretion of OT was elicited by the excessive dilation of the vaginal wall with the speculum. By comparison, mating did not evoke a period of uterine hyperactivity and respects the physiological post-coital resting period.

Adrenergic alpha-Antagonists↗
PubMed1989

Catecholamines, oxytocin and milk removal in dairy cows.

Experiments were designed to study the effects of catecholamines on oxytocin responses and milk removal in dairy cows. Adrenalin, noradrenalin, dopamine, isoproterenol (a beta-adrenoceptor agonist), phentolamine (an alpha-adrenergic blocker) and propranolol (a beta-adrenergic blocker) were infused intravenously. In addition, adrenalin was infused together with phentolamine and/or propranolol. Infusions started 8 min before milking and lasted until the end of milking. In some cases electroshocks (for 5 s) were applied immediately before milking in the absence and presence of phentolamine and propranolol. Adrenalin, noradrenalin and dopamine reduced milk removal, but only if administered in supraphysiological amounts. The effect of adrenalin and electroshocks on milk removal could be inhibited only partly by phentolamine. Inhibition of milk removal was not mediated by reduced oxytocin responses. Enhanced local release of catecholamines from sympathetic nerves was presumably responsible for lowered milk removal in response to electroshocks. Milk removal was facilitated during alpha-adrenergic blockade and during beta-adrenoceptor stimulation.

Animals↗
PubMed1987

Intra-arterial vasodilator agents to reverse human finger vasoconstriction.

Persistent vasospasm of the digits is difficult to attenuate or reverse. We studied the effect of intra-arterial nitroprusside on humoral and neurogenic digital vasoconstriction. Fingertip blood flow (FBF) was measured by venous occlusion plethysmography and capillary flow (CF) by the disappearance rate of a local injection of radioisotope. Small doses of nitroprusside (1 to 2 micrograms/min) increased FBF in fingers vasoconstricted by intra-arterial norepinephrine (4.7 +/- SE 1.7 to 38.4 +/- 26 ml min-1 100 ml-1 of tissue). Large doses of nitroprusside (up to 40 micrograms/min) did not increase FBF (11.8 +/- 6.0 ml to 6.6 +/- 3.9 ml) in fingers vasoconstricted by sympathetic nerve stimulation (body cooling). Forearm blood flow was measured in six subjects in the cool room and all showed an increase in flow with nitroprusside (6.7 +/- 1.1 ml to 26.0 +/- 6.0 ml), demonstrating that effective doses were used. Nitroglycerin (2.5 to 5 micrograms/min) significantly increased FBF from 5.1 +/- 1.9 ml to 14.8 +/- 6.9 ml as did phentolamine (50 to 100 micrograms/min) from 6.7 +/- 2.8 ml to 36.0 +/- 11.3 ml in sympathetically vasoconstricted subjects. Only phentolamine increased CF significantly (0.8 +/- 0.2 ml to 2.8 +/- 0.6 ml). Nitroprusside is an effective vasodilator for humorally induced vasoconstriction, but sympathetic digital vasoconstriction is resistant to nitroprusside and nitroglycerin is less effective than phentolamine. Phentolamine is the preferred agent because it increased FBF and CF.

Female↗
PubMed1999

Effects of A1-adenosine receptor antagonists on purinergic transmission in the guinea-pig vas deferens in vitro.

1. Intracellularly recorded excitatory junction potentials (ej.ps) were used to study the effects of adenosine receptor antagonists on neurotransmitter release from postganglionic sympathetic nerve terminals in the guinea-pig vas deferens in vitro. 2. The A1 adenosine receptor antagonists, 8-phenyltheophylline (10 microM) and 8-cyclopentyl-1,3-dipropylxanthine (0.1 microM), increased the amplitude of e.j.ps evoked during trains of 20 stimuli at 1 Hz in the presence, but not in the absence, of the alpha2-adrenoceptor antagonist, yohimbine (1 microM) or the non-selective alpha-adrenoceptor antagonist, phentolamine (1 microM). 3. Adenosine (100 microM) reduced the amplitude of e.j.ps, both in the presence and in the absence of phentolamine (1 microM). This inhibitory effect of adenosine is most likely caused by a reduction in transmitter release as there was no detectable change in spontaneous ej.p. amplitudes. 4. In the presence of phentolamine, application of the adenosine uptake inhibitor, S-(p-nitrobenzyl)-6-thioinosine (0.1 microM), had no effect on ej.p. amplitudes. 5. The phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine (100 microM), significantly increased the amplitudes of all e.j.ps evoked during trains of 20 stimuli at 1 Hz, both in the presence and in the absence of phentolamine (1 microM). 6. These results suggest that endogenous adenosine modulates neurotransmitter release by an action at prejunctional A1 adenosine receptors only when alpha2-adrenoceptors are blocked.

1-Methyl-3-isobutylxanthine↗
PubMed1995

Effects of imidazoline compounds on cytoplasmic Ca2+ concentration and ATP-sensitive K+ channels in pancreatic B-cells.

Phentolamine, an alpha-adrenoceptor-blocking agent with an imidazoline structure, induces an increase in the cytoplasmic Ca2+ concentration of pancreatic B-cells. This effect occurs at a concentration (32 microM) at which phentolamine is able to enhance glucose-induced insulin secretion. The increase in cytoplasmic Ca2+ concentration caused by phentolamine is additive to the one elicited by a maximally effective concentration of tolbutamide (100 microM). Imidazoline-binding sites in insulin-secreting HIT cells can also be occupied by the guanidinium compound guanabenz, which was found to be a potent and reversible blocker of ATP-dependent K(+)-channels in B-cells. In contrast to phentolamine, guanabenz blocks the ATP-dependent K(+)-channels only in the inside-out mode, but not in the cell-attached mode of the patch-clamp technique. In conclusion, imidazolines and structurally related compounds block ATP-dependent K(+)-channels by binding to the cytoplasmic face of the plasma membrane, and may have effects on other ion channels which contribute to the elevation of cytoplasmic Ca2+ concentration and, consequently, to insulin release.

Adenosine Triphosphate↗
PubMed1984

Adrenergic effects on plasma levels of glucagon, insulin, glucose and free fatty acids in rabbits.

Adrenergic effects on plasma levels of glucagon, insulin, glucose and free fatty acids were studied in fasted rabbits by infusing epinephrine, norepinephrine, isoproterenol, phentolamine (an adrenergic alpha-receptor blocking drug) and propranolol (an adrenergic beta-receptor blocking drug). The adrenergic effects on the plasma levels of insulin, glucose and free fatty acids were similar to those found in other species. The plasma levels of insulin were increased by beta-receptor stimulation (isoproterenol, phentolamine + epinephrine) and decreased by alpha-receptor stimulation (epinephrine, norepinephrine, propranolol + epinephrine). The plasma levels of glucose were increased by both alpha- and beta-receptor stimulation, and the epinephrine-induced hyperglycaemia was only blocked by combined infusions with phentolamine and propranolol. The plasma levels of free fatty acids were increased by saline and further increased by beta-receptor stimulation (isoproterenol), while epinephrine and norepinephrine gave variable results. Alpha-receptor stimulation (propranolol + epinephrine) slightly decreased the plasma levels of free fatty acids. The plasma levels of glucagon, however, were mainly increased by alpha-receptor stimulation (epinephrine, norepinephrine, propranolol + epinephrine) and increased only to a minor extent by beta-receptor stimulation (isoproterenol, phentolamine + epinephrine) in rabbits. This is in contrast to results reported for humans, where beta-receptor stimulation seems to be most important in stimulating glucagon release.

Animals↗
PubMed1981

Adrenergic modulation of glucagon and insulin secretion in obese and lean humans.

The adrenergic modulation of immunoreactive insulin (IRI) and glucagon (IRG) secretion was studied in 5 massively obese subjects hospitalized ion a metabolic ward. Epinephrine was infused alone or in combination with propranolol, a beta adrenergic blocking drug, or with phentolamine, an alpha adrenergic blocking drug. Epinephrine infusion produced a significant (p less than .02) rise in IRG levels which was blocked by addition of either phentolamine or propranolol. Pure alpha adrenergic stimulation with propranolol-epinephrine infusion inhibited IRG secretion (p less than .02). IRI levels decreased with propranolol-epinephrine infusion (p less than .02), increased with phentolamine-epinephrine infusion, and were not affected by infusion of epinephrine alone. Glucose concentrations rose with all 3 infusions but were less with phentolamine-epinephrine. A control group of 4 lean outpatients on a ad lib diet demonstrated a similar pattern but the changes of IRG secretion were smaller than in the obese subjects and were not statistically significant. We conclude that in obese humans IRI secretion is increased by beta adrenergic stimulation, is decreased by alpha adrenergic stimulation, and is unaffected by combined alpha and beta adrenergic stimulation. In contrast, IRG secretion is stimulated by combined alpha and beta adrenergic stimulation, is inhibited by pure alpha adrenergic stimulation, and is unaffected by pure beta adrenergic stimulation.

Adult↗
PubMed1985

Influence of alpha-adrenergic blockade on platelet-mediated thrombosis in stenosed canine coronary arteries.

The functional significance of platelet alpha-adrenergic receptors in vivo is uncertain. The aim of this study was to elucidate their role in experimental coronary thrombosis. In 46 open-chest dogs with a critical coronary stenosis produced by plicating the coronary artery wall with a suture, blood flow showed cyclical reductions followed by an abrupt return to control levels. The flow reduction were previously shown to be caused by platelet aggregation. In the present study they were unaffected by heparin (1,000 U . kg-1 . h-1) at the start of the experiment but consistently abolished by aspirin (30 mg . kg-1) at the end of the protocol, further supporting platelet aggregation as the primary mechanism. After 1 h of observation, dogs were assigned to one of the following groups: control (no intervention, n = 9), phentolamine (a nonselective alpha-blocker) "low dose" (0.07 mg . kg-1 bolus followed by 0.1 mg . kg-1 . min-1, n = 4), phentolamine "high-dose" (3 mg . kg-1 bolus followed by 0.07 mg . kg-1 . min-1, n = 6), prazosin (an alpha 1-blocker, 2 mg . kg-1, n = 8), yohimbine (an alpha 2-blocker, 3 mg . kg-1, n = 11) or prazosin + yohimbine (same doses, n = 8). In controls, cyclical reductions in flow continued unchanged for another hour. Phentolamine effected a partial dose-related inhibition of flow reductions; however, prazosin and yohimbine, given separately or in combination, failed to produce any significant effect despite an alpha-blocking action equivalent to or greater than that of phentolamine (alpha-agonist dose-response studies).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1992

Effects of alpha and beta adrenergic blockade on coronary arterial microvessels in the beating canine heart.

OBJECTIVE: The aim was to clarify the effects of alpha and beta adrenergic blockade on coronary arterial microvessels and to assess the role of alpha and beta adrenergic tone in normally beating hearts. METHODS: 47 anaesthetised open chest dogs were studied. The diameters of epicardial arterial microvessels were measured in beating hearts using an incident light fluorescence microscope equipped with a floating objective. Drugs were infused into the left anterior descending coronary artery keeping the heart rate and aortic pressure at control levels. To examine the effect of alpha adrenergic blockade, phentolamine (100 micrograms.kg-1) was given in the absence or presence of beta adrenergic blockade (propranolol 50 micrograms.kg-1). To examine the effect of beta adrenergic blockade, propranolol (50 micrograms.kg-1) or three doses of ICI 118,551 (a selective beta 2 antagonist, 0.1, 0.5, and 1.0 microgram.kg-1.min-1) was given. RESULTS: Coronary arterial microvessels were divided into three groups according to the control diameters (D) of small (D less than 100 microns), medium (100 less than or equal to D less than 200 microns) and large (D greater than or equal to 200 microns) groups. In the absence of beta adrenergic blockade, phentolamine significantly dilated all vessel groups: small +19.6 (SEM 5.6)%, medium +5.8(2.3)%, large +5.3(0.9)%. In the presence of beta adrenergic blockade, the vasodilator effect of phentolamine was completely abolished. Propranolol constricted all vessel groups: small -3.6(1.1)%, medium -4.8(1.0)%, large -3.5(1.0)%. ICI 118,551 significantly constricted the large vessel group [-2.5(0.6)%] at the mid dose, and the medium and large vessel groups [medium -3.1(0.8)%, large -3.5(1.3)%] at the highest dose. CONCLUSIONS: These data indicate that (1) the vasodilator effect of phentolamine is induced by beta adrenergic stimulation; (2) resting alpha adrenergic tone of coronary arterial microvessels is minimal in normally beating hearts, and (3) resting beta adrenergic tone may play a physiological role in coronary arterial microvessels, and beta 2 adrenergic tone predominates in arterial microvessels greater than 100 microns in diameter.

Adrenergic alpha-Antagonists↗
PubMed1989

Treatment of peripheral ischemia secondary to lidocaine containing epinephrine.

Accidental injection of local anesthetics containing epinephrine into a digit can cause distal tissue necrosis. Norepinephrine infiltration in subcutaneous tissue also causes tissue necrosis. Phentolamine has been used to prevent necrosis from norepinephrine. Because both epinephrine and norepinephrine are alpha- and beta-adrenergic stimulators, the rat foot model was developed to study the possible use of phentolamine or labetalol in protection against tissue necrosis after injection of epinephrine in the extremity. Phentolamine was found to be useful in preventing tissue necrosis after the injection of local anesthetic containing epinephrine in the skin of the rat foot. Labetalol was found to be less effective in preventing tissue necrosis. Phentolamine may be useful in preventing tissue necrosis after the inadvertent injection of epinephrine containing local anesthetics in the digit.

Animals↗
PubMedDate not supplied

Presynaptic modulation of heart rate responses to cardiac nerve stimulation in pithed rats.

The effects of presynaptic alpha-adrenoceptor blockade with phentolamine, before and after inhibition of uptake-1 with cocaine, on the positive chronotropic response to cardiac sympathetic nerve stimulation in pithed rats was investigated. Phentolamine or cocaine each enhanced the cardiac responses to stimulation at 1 Hz for 15 sec by 10-25%; the combination of the drugs caused no greater enhancement than did either drug alone. Cocaine considerably potentiated the tachycardia produced during prolonged stimulation at 0.1 but not at 0.2-1 Hz. Phentolamine potentiated the responses to stimulation at 0.2 and 0.5 Hz by 21 and 12%, respectively, but not those at 0.1 or 1 Hz. After cocaine, phentolamine caused a further small increase in the response at 0.1 Hz but not other frequency. It is concluded that presynaptic alpha-adrenoceptors exert only modest control over the responses of the rat heart to cardiac nerve stimulation and that this modulation is little influenced by uptake-1.

Animals↗
PubMedDate not supplied

Mediation of renin release in essential hypertension by alpha-adrenoreceptors.

We studied the role of alpha-adrenoceptors in controlling renin release by infusing increasing doses of phentolamine into six patients with essential hypertension. Furthermore, in order to evaluate the relative importance of alpha 1- and alpha 2-adrenoceptors, phentolamine infusion was repeated in the same patients after pretreatment with prazosin, a selective alpha 1-blocking agent, and oxprenolol, a nonselective beta-blocker. After placebo, phentolamine infusion did not change mean blood pressure or heart rate and increased plasma renin activity (PRA) in a dose-dependent fashion. This finding suggests that the drug acts directly on the intrarenal renin producing apparatus and seems to confirm the inhibitory role of alpha-adrenoceptors in the control of renin release. After prazosin and oxprenolol pretreatment, PRA was respectively increased and decreased but it was unmodified by phentolamine infusion. This latter finding may indicate that both alpha 1- and alpha 2-adrenoceptors are involved in renin release or that alpha-adrenoceptors cannot be clearly differentiated into alpha 1- and alpha 2-subtypes.

Adult↗
PubMedDate not supplied

In vitro evidence for dopaminergic receptors in human renal artery.

Effects of dopamine on human renal arteries were pharmacologically investigated in vitro. Norepinephrine (5 X 10(-10)-5 X 10(-5) M) produced concentration-dependent contractions of isolated renal arterial strips, which were significantly depressed by prior administration of phentolamine or phenoxybenzamine. Isoproterenol (4 X 10(-10)-4 X 10(-6) M) concentration dependently relaxed the strips under potassium contracture, but a high dose (4 X 10(-5) M) constricted them. Biphasic responses to isoproterenol were changed to concentration-dependent contractions by prior administration of propranolol, and abolished by propranolol together with phentolamine. Dopamine (5 X 10(-8)-5 X 10(-4) M) produced concentration-dependent contractions of human renal arteries, which were not significantly influenced by propranolol but which were reversed to relaxations by phentolamine. Dopamine-induced relaxations, which were obtained after administration of phentolamine, were not significantly affected by propranolol, but were significantly depressed by combined application of propranolol and haloperidol, or of propranolol and droperidol. Results suggest that isolated human renal arteries have dopaminergic receptors in their smooth muscles which show relaxations of renal arteries after alpha-adrenoceptor blockade.

Adult↗
PubMed1988

Alpha-adrenoceptor influence on plasma levels of neuropeptide Y-like immunoreactivity and catecholamines during rest and sympathoadrenal activation in humans.

Antecubital venous plasma neuropeptide Y-like immunoreactivity (NPY-LI) and catecholamines were analyzed in six healthy volunteers performing a graded bicycle exercise without medication and after acute administration of clonidine, phentolamine, and nifedipine. During the control exercise, plasma noradrenaline (NA), adrenaline (A), and NPY-LI increased to 17-, 7-, and 3-fold the resting values, respectively, at a maximal workload. Clonidine (300 micrograms p.o.) reduced resting and exercising heart rate (HR) and systolic blood pressure (SBP). Plasma NA at rest decreased and NA, A, and NPY-LI were 40-60% lower during the exercise after clonidine compared to the control. Phentolamine (0.07 mg X kg-1 every 10 min i.v.) and nifedipine (20 mg p.o.) increased HR and reduced SBP during the exercise. Plasma NA at rest was elevated threefold and the exercise-induced increases in NA and A were also enhanced after phentolamine. Plasma NPY-LI at rest was unchanged by phentolamine, while it was increased five-fold, as compared to the control, at the highest workload. Nifedipine slightly enhanced plasma NA and NPY-LI but not A during exercise. It is suggested that NPY is released mainly at high levels of sympathetic activity and that blood-pressure-lowering drugs acting on alpha adrenoceptors acutely influence the release of both NA and NPY-LI from sympathetic nerves in humans.

Adrenal Glands↗