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PubMed1991

Disruption of GnRH pulses by anti-GnRH serum and phentolamine obliterates pulsatile LH but not FSH secretion in ovariectomized rabbits.

It has been hypothesized that the secretion of gonadotropins, i.e. luteinizing hormone (LH) and follicle-stimulating hormone (FSH), is driven by a synchronized neural network ('pulse generator'). This network, regulated in part by alpha-adrenergic activity, ultimately generates bursts of hypothalamic gonadotropin-releasing hormone (GnRH) release. In this study, we used the push-pull (PP) perfusion technique in ovariectomized rabbits to investigate three aspects of the ('GnRH/gonadotropin pulse generator') hypothesis. The objectives were to determine: (1) if plasma LH and FSH pulses occur concomitantly with mediobasal hypothalamic (MBH-) GnRH pulses, (2) changes in the patterns of pulsatile LH and FSH secretion when pulsatile MBH GnRH signals are interrupted by either local immunoneutralization of GnRH or intravenous infusion of the alpha-adrenergic antagonist phentolamine (PHEN, 4 mg/kg BW), and (3) whether third cerebroventricular (3VT-) GnRH patterns reflect neuronal GnRH release from the MBH. We found that while both plasma LH and FSH patterns were pulsatile, MBH GnRH pulses were significantly coupled only with LH pulses (94% coincidence). Both the local immunoneutralization of MBH GnRH pulses and the PHEN-induced suppression of MBH GnRH pulses obliterated the pulsatile secretion of LH, but not FSH. Neither MBH GnRH nor plasma LH or plasma FSH pulses were concurrent with 3VT GnRH pulses. However, the PP perfusion of the 3VT appeared to alter the pulsatile release of MBH GnRH and pituitary LH. The results support the hypothesis that in the absence of ovarian signals, the 'pulse generator' is maintained by tonic alpha-adrenergic input and that a 'cellular unity' of MBH GnRH release (GnRH pulses) drives the gonadotrophs to secrete LH in pulses. In contrast, the pulsatile release of FSH appears to involve additional nonovarian regulatory events to those controlling LH secretion.

Animals↗
PubMed1993

Effects of clonidine and phentolamine infused into the medial preoptic area and medial basal hypothalamus of the guinea pig.

In ovariectomized (OVX) female guinea pigs sequential administration of estradiol and then progesterone (P) is usually necessary to induce the sexually receptive lordosis posture. Systemic administration of alpha-adrenergic agonists can induce lordosis in OVX guinea pigs primed with estradiol benzoate (EB) alone and facilitate lordosis in OVX females primed with EB and P. In this study, we examined the regional specificity of this regulation by infusing the alpha-adrenergic agonist clonidine (CLON) or the alpha-adrenergic antagonist phentolamine (PHEN) into discrete brain areas. CLON, infused in the medial basal hypothalamus (MBH) of EB-primed females, increased the percentage of females showing lordosis 15-45 min after infusion (p < 0.05) and also increased the number of seconds females held the lordosis posture 15 min to approximately 2.0 h after infusion (by as much as 65% at 15 min p < 0.001). CLON infused in the medial preoptic area (MPOA) of EB primed females had no effect on lordosis except at 4.0 h after infusion when it increased the number of seconds females held the lordosis posture (p < 0.05). In EB + P primed females, PHEN infused into the MBH transiently reduced the number of seconds EB + P primed females held lordosis from 30 min to approximately 2.0 h after infusion (by as much as 64% at 1.0 h; p < 0.01). Conversely, PHEN infused into the MPOA of EB + P primed females transiently increased the number of seconds females held lordosis from 15 min to 2.0 h after infusion (maximum difference 64%; p < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗
PubMed1988

Diagnosis and therapy of erectile dysfunction using papaverine and phentolamine.

The introduction in 1982 of vasoactive agents for intracavernous injection represents a milestone in the diagnosis and treatment of erectile dysfunction. Two preparations, the single drug papaverine hydrochloride and the combination of phentolamine mesylate and papaverine hydrochloride, hold great promise. In the last few years, the use of vasoactive drugs for evaluation and treatment of erectile dysfunction has become accepted worldwide. This paper explores the diagnostic and therapeutic possibilities and hazards implied in the method, assessing the advantages and drawbacks of papaverine and the combination product.

Drug Therapy, Combination↗
PubMed1976

Pharmacological mechanisms for left ventricular unloading in clinical congestive heart failure. Differential effects of nitroprusside, phentolamine, and nitroglycerin on cardiac function and peripheral circulation.

We compared cardiocirculatory actions of the commonly employed systemic vasodilators, intravenous (iv) nitroprusside (NP), iv phentolamine (PH), and sublingual nitroglycerin (NTG), causing left ventricular (LV) unloading in 29 chronic coronary subjects with congestive failure to determine whether they produce disparate responses in LV function by different relaxing actions on systemic resistance and capacitance beds. Each drug equally lowered systemic arterial pressures to a small extent, whereas heart rate rose slightly with NTG. Cardiac catheterization showed a decline in end-diastolic pressure with NTG (19 to 8 mm Hg) which was greater (P less than 0.05) than with NP and PH (21 to 11). Cardiac index increased (P less than 0.05) during NP (2.68 to 2.93 liters/min per m2) and PH (2.60 to 3.02) but was unchanged (2.83) by NTG. Stroke work increased with PH, ejection fraction rose with NP and PH, and mean ejection rate increased with each, whereas pressure-time per minute fell and end-diastolic volume decreased with each agent. Total systemic vascular resistance declined (P less than 0.001) during NP and PH (1,475 to 1,200 dynes sec cm-5) but was unchanged (1,487) by NTG. Plethysmographically, forearm vascular resistance (FVR) decreased (P less than 0.01) with NP and PH (61.6 to 39.1 mm Hg/ml per 100 g/min) but not (52.4) by NTG. The decreases in venous tone (VT) with NTG (18.2 to 9.3 mm Hg/ml) and NP (18.5 to 9.8) were greater (P less than 0.05) than with PH (18.8 to 13.1) FVR/VT percent changes of 0.96, 1.62, and 0.53 with NP, PH, and NTG indicated balanced systemic arteriolovenous relaxation by iv NP, greater arteriolar dilation with iv PH, and predominant venous dilation by sublingual NTG. Thus, vasodilators produce disparate modifications of LV function by their differing alterations of preload and impedance, which are dependent upon relative extents of relaxation of systemic resistance and capacitance vessels characteristic of each agent as used clinically.

Adult↗
PubMedDate not supplied

The effect of phentolamine on conduction in the bundle of His.

A His bundle electrogram was obtained in a 65 year old male with syncopal episodes. A split bundle of His deflection was recorded. After the intravenous administration of phentolamine, a marked shortening of the H-H' interval was observed. This signifies an improvement in conduction at the bundle of His level.

Aged↗
PubMed1976

Phentolamine blocks the somatostatin-mediated inhibition of insulin secretion.

This study was undertaken to determine the influence of alpha-adrenergic blockade upon the somatostatin-mediated inhibition of insulin secretion. Somatostatin inhibited both the basal and glucose-stimulated pancreaticoduodenal vein insulin output of dogs. This effect was not observed during a simultaneous infusion of phentolamine, an alpha-adrenergic blocker. It is proposed that alpha-adrenergic mechanisms play a role in the inhibition of insulin secretion by somatostatin.

Animals↗
PubMed1987

Effects of phentolamine on response to supine leg exercise of peripheral venous pressure and plasma catecholamine concentration--a study in patients with mild congestive heart failure.

The present study examined the effects of phentolamine (PH) on the increments in peripheral venous pressure (delta VP), and of plasma noradrenaline (delta NA) and adrenaline (delta A) concentration, in response to supine leg exercise. Peripheral venous pressure and plasma catecholamine concentrations were measured at rest and during exercise, before and after intravenous injection of PH (0.1 mg/kg) in 10 healthy volunteers (Group C), and in 42 patients with primarily left-sided heart diseases but without apparent right-sided or left-sided heart failure (NYHA class I, II). These cardiac patients were divided into 2 groups on the basis of delta VP. Those with delta VP below 35 mmH2O comprised the normal group (Group N), and those with delta VP more than 35 mmH2O the abnormally high group (Group H). 1) In Group C, delta VP changed only slightly from 11.1 +/- 2.8 (mean +/- SE) to 4.9 +/- 1.7 mmH2O with an intravenous injection of PH. On the other hand, PH caused a significant decrease in delta VP from 22.2 +/- 2.3 to 10.4 +/- 2.3 mmH2O in Group N (p less than 0.001), and from 52.7 +/- 3.4 to 17.0 +/- 12.4 mmH2O in Group H (p less than 0.001). It was suggested that PH blocked the alpha-receptors of the systemic capacitance vessels, thereby inhibiting the constriction of these vessels. 2) Both NA at rest and delta NA before PH were significantly higher in Group H than those in Groups C or N. delta NA increased significantly after the PH injection in all 3 groups, i.e., from 0.038 +/- 0.013 (mean +/- SE) to 0.282 +/- 0.051 ng/ml in Group C, from 0.056 +/- 0.013 to 0.279 +/- 0.034 ng/ml in Group N and from 0.279 +/- 0.034 to 0.839 +/- 0.103 ng/ml in Group H. The increase in delta NA after PH was especially marked in Group H. It was suggested that the "sympathetic nervous activity" was increased in the patients with an impaired left ventricular pumping function. 3) PH caused a slight increase in delta A in all groups, but there was no significant difference in delta A before and after PH in the 3 groups.

Adult↗
PubMed1989

Increase in plasma noradrenaline concentration after the administration of phentolamine in the patients with "latent" left-sided heart failure.

We measured increments of peripheral venous pressure induced by dynamic leg exercise (delta VP) in 10 healthy subjects (Group C) and 70 patients with heart diseases which primarily affect the left-side of the heart. None of the subjects showed apparent symptoms of left- or right-sided heart failure. The patients were divided into 2 groups on the basis of delta VP, namely, Group N (delta VP less than 35 mmH2O, n = 30, normal reaction) and Group H (delta VP greater than or equal to 35 mmH2O, n = 40, abnormal reaction). We measured the increments of plasma concentrations of noradrenaline (delta NAPH) and adrenaline (delta APH) with infusion of phentolamine (PH). Parallel studies with nitroglycerin and prazosin supplied strong evidence that delta NAPH was brought about mainly by the blockade of alpha 2-receptors at the sympathetic nerve terminals. Thus, we estimated the degree of sympathetic nerve activity from the central nervous system by opening using PH the negative feed-back loop for noradrenaline (NA) release at the sympathetic nerve terminals, and this degree of sympathetic nerve activity was compared with the degree of delta VP. The results obtained were 1) there was a rough overall correlation between delta VP and delta NAPH in the subjects of Groups C, N and H, and 2) delta NAPH was significantly higher in Group H than in Groups C and N. These results suggest that much reliance can be placed on the measured increment of plasma NA concentration in response to the administration of PH in assessing the degree of enhanced sympathetic nerve activity in the patients with "latent" left-sided heart failure.

Adult↗
PubMed1992

The effects of phentolamine and nitroglycerin on right-sided hemodynamics in cardiac patients can be explained by a shift of the systemic venous return curve and right-ventricular output curve.

The present study investigated the effects of phentolamine (PH) and nitroglycerin (NG) on the hemodynamics of the right heart in patients with cardiac disease. The patients were divided into a well-functioning left heart group (W group, n = 15) and a poorly-functioning left heart group (P group, n = 15). Right cardiac hemodynamic parameters and plasma noradrenaline (NA) and adrenaline (A) concentrations were measured before and after administering PH (0.1 mg/kg, i.v.) or NG (0.6 mg, sublingual). In a parallel animal study we obtained a systemic venous return curve by measuring mean circulatory pressure (MCP), mean right atrial pressure (RAP) and cardiac output, before and after administering PH (0.1 mg/kg, i.v.) or NG (12.5 micrograms/kg, i.v.) to anesthetized open-chest dogs (n = 14). We used MCP data (W group: 7.5 mmHg, P group: 10 mmHg) obtained in a separate series of human studies in our laboratory. We constructed the venous return curve by connecting the MCP point on abscissa with the cardiac index (CI)-RAP plot obtained in the clinical study. We also constructed the right ventricular output curve by connecting the point of -2 mmHg on the abscissa with the CI-RAP plot. We obtained the following results: (1) PH shifted the CI-RAP plot to the left and upwards, while NG shifted the CI-RAP plot to the left almost horizontally on the CI-RAP plane, where CI was plotted on ordinate and RAP on abscissa. The length [formula: see text] C = control point, PH = point after PH) of the shift of CI-RAP plot due to PH was greater in the P group than in W group, while there was no difference in the length [formula: see text] C = control point, NG = point after NG) of the shift of CI-RAP plot due to NG between P and W groups. (2) Both PH and NG significantly elevated plasma NA and A concentrations in both the W and P groups. In the P group, PH increased the plasma NA concentration significantly more than did NG, but both drugs increased plasma A concentration to a similar extent. (3) Both PH and NG significantly decreased the mean pulmonary arterial pressure with NG doing so significantly more than PH.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1988

Preventive action of phentolamine on adrenaline induced blood glucose elevation in humans.

A comparison of the action of adrenaline infusion and a combined adrenaline + alpha blocker (phentolamine, Regitine) infusion on blood glucose (BG), plasma immunoreactive insulin (IRI), BG/IRI ratio, C-peptide, and plasma cortisol levels was made in healthy young human subjects. The purpose of the experiment was to check, whether alpha block could abolish adrenaline-induced enhancement of blood glucose levels. The results show that during enhanced adrenaline levels, the use of regitine could indeed normalize blood glucose levels, not so much by increasing the IRI secretion, but by diminishing adrenaline-induced liver glycogenolysis via alpha receptors. This could be a model to prevent stress (adrenaline) induced metabolic deviations in diabetics, especially before and during predictable stress situations, e.g. examinations or surgery.

Adrenergic alpha-Antagonists↗
PubMed1978

Comparative vasodilator effects of nitroprusside, phentolamine, and nitroglycerin on hemodynamics, regional myocardial function and epicardial electrogram in dogs with acute myocardial ischemia.

The effects of nitroprusside (NP), phentolamine (PH), and nitroglycerin (NTG) were studied on systemic hemodynamics, regional contraction and epicardial ST segment in the border and non-ischemic zones of the left ventricle of anesthetized open chest dogs. The anterior descending coronary artery (LAD) was completely occluded. NP (5 microgram/Kg/min) or PH (100 microgram/Kg/min) was drip-infused, or a bolus injection of NTG (20 microgram/Kg) was administered intravenously. The 3 vasodilator agents produced somewhat similar reductions in systemic arterial pressure. However, NP caused a greater reduction in total peripheral resistance (TPR) than in left ventricular end-diastolic pressure (LVEDP), and caused a decline, in the ischemic marginal zone, in both ST segment eievation and paradoxical systolic lengthening. PH decreased TRP without reducing LVEDP and elevated the ST segment. NTG markedly reduced LVEDP and TPR slightly. NTG improved the elevated ST segment and paradoxical systolic expansion of the segmental myocardium in the border zone. Cardiac output rose with NP and PH, whereas injected NTG caused a reduction in cardiac output. These findings suggest that NP favourably affects the ischemic myocardium mainly by reducing the afterload and that the NTG-induced improvement of myocardial ischemia can be attributed mainly to preload reduction, while PH enhances cardiac function with slight or no improvement of myocardial ischemia in the border zone.

Acute Disease↗
PubMed1997

Hemodynamic effects of nicardipine and phentolamine in combination with norepinephrine in a canine low-output-state model.

Norepinephrine (NE) is one of the most potent positive inotropic drugs available for the treatment of low-output state following open-heart surgery. However, its inotropic effect is often masked by a significant increase of peripheral vascular resistance due to marked vasoconstriction. The purpose of the present study was to investigate whether the use of nicardipine (Nc) and phentolamine (Ph) in combination with NE could ameliorate the adverse vasoconstrictive action of NE. A low-output-state (LOS) model was produced by global myocardial ischemia due to electrically induced intermittent ventricular fibrillations in open-chest dogs. Twenty-eight dogs were divided into 6 groups according to the drugs infused after producing LOS. In the control group, hemodynamic changes similar to the clinical low-output state were observed, e.g., a decrease in cardiac output (CO) and left ventricular dp/dt, and an increase in the systemic vascular resistance (SVR). The use of NE alone produced marked increases in the systemic arterial pressure (SAP), heart rate, and SVR, with a slight increase in CO. The infusion of Nc alone produced decreases in SVR and SAP with a slight increase in CO. The concomitant infusion of NE and Nc produced increases in SV and CO, and decreases in SAP and SVR. The infusion of Ph alone produced no significant hemodynamic changes. The combined use of NE and Ph produced increases in CO, SAP and heart rate, but not to a significant extent. These results suggest that there are major advantages in the concomitant use of NE and Nc for the control of LOS.

Animals↗
PubMed1988

Effects of the alpha-adrenoceptor antagonists phentolamine, phenoxybenzamine, and idazoxan on sympathetic blood flow control in the periodontal ligament of the cat.

Blood flow changes in the periodontal ligament (PDL) were measured indirectly by monitoring the local clearance of 125I- during electric sympathetic nerve stimulation or close intra-arterial infusions of either noradrenaline (NA) or adrenaline (ADR) before and after administration of phentolamine (PA), phenoxybenzamine (PBZ), or Idazoxan (RX). At the doses used in the present study, PA was the only antagonist that significantly reduced the blood flow decrease seen on activation of sympathetic fibers, although PBZ also reduced this response. Idazoxan, however, did not induce the consistent effect on blood flow decreases seen on sympathetic activation. All three alpha-adrenoceptor antagonists almost abolished the effects of exogenously administered NA and ADR. The results suggest the presence of functional post-junctional adrenoceptors of both the alpha 1 and alpha 2 subtypes in the sympathetic regulation of blood flow in the PDL of the cat. A component of the response elicited by electrical sympathetic stimulation appeared to be resistant to alpha-adrenoceptor blockade. Administration of guanethidine (which inhibits further release of NA and neuropeptide Y) after PA abolished this residual sympathetic response.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

[Effect of phentolamine and anaprilin on the makeup and distribution of electrolytes in the myocardium].

Acute tests with rats demonstrated that the adrenoblocking agent phentolamine acts predominantly on the potassium level in the myocardium, raising its total, intra- and extra-cellular content. The effect of anapriline was mainly on sodium. Thyramine, which like adrenoblocking agents displays a catecholine-reducing effect, did not produce any similar changes in the potassium and sodium content.

Animals↗
PubMed1992

[Inhibition of dopamine on WDR neurons of dorsal horn not antagonized by phentolamine and naloxone in rats].

The inhibitory effects of dopamine (DA) applied spinally on the wide dynamic range (WDR) neurons of dorsal horn in rats were studied with extracellular recording technique. 54 WDR units were tested from 43 rats. With a dosage of DA from 0.26 x 10(-6) to 1.58 x 10(-6) mol/kg, the inhibitory effect of the neurotransmitter on the responses of dorsal horn neurons to noxious transcutaneous electrical stimulation exhibited a gradual increase. After DA (0.52 x 10(-6) mol/kg) administration, the inhibitory effect of DA began to appear in 5 min and reach to maximum in 15 min, whereupon the maximum level could be maintained for about 25 min. This effect of DA could be reversed completely by dopaminergic receptor antagonist, droperidol (0.66 x 10(-6) mol/kg) but not by 2.65 x 10(-6) mol/kg phentolamine or 1.37 x 10(-6) mol/kg naloxone. The results of the present investigation suggest that DA may be involved in the modulation of nociception at the spinal level as an independent neurotransmitter.

Animals↗
PubMed1977

[Phentolamine and dibenamine action on the carotid reflexes induced by lobeline].

On the carotid reflexogenic zone lobeline provoques : 1) a increase of amplitude and rate of respiratory movements with bradycardia and hypotension ; 2) a secondary decrease of amplitude and rate of breathing with tachycardia. Acting on the reflexogenic zone, phentolamine and dibenamine provoque a transitory weakening or disappearance of these reflexes. These effects are induced by a local action, because they are not observed by intravenous injection of the drugs and the lobeline reflexes starting from the carotid sinus of the other side are not affected.

Animals↗
PubMed1990

[Hypothermia after cardiopulmonary bypass in man: effects of prostaglandin E1 and phentolamine].

The "afterdrop" in body temperature (TEMP) following adequate rewarming from hypothermic cardiopulmonary bypass (CPB) is frequently observed. This temperature drop sometimes accompanied by shivering results in increased myocardial oxygen demand. We investigated the relations between the afterdrop and use of vasodilators after CPB. For vasodilator therapy, PGE1 at the rate of 0.025-0.088 microgram.kg-1.min-1 (Prostaglandin Low Doses, PLD; n = 8), 0.107-0.136 microgram.kg-1.min-1 (Prostaglandin High Doses, PHD; n = 7), or phentolamine at 4.1-5.9 micrograms.kg-1.min-1 (PHENT; n = 8) were intravenously infused in 23 adult patients after CPB. During three hour period after CPB, esophageal, rectal, and forehead TEMP are lower in PHENT than in PGE1 groups. There were significant differences between PHD and PHENT group. Finger tip TEMP was lower in PGE1 groups than in PHENT group. There were significant differences between PHD and PHENT group. There were no differences in systemic arterial pressure, cardiac index (CI) and systemic vascular resistance (SVR) at any point between PHD and PHENT groups. It is concluded that PHENT increases the peripheral skin blood flow and TEMP but decreases the visceral TEMP possibly due to vasodilatation of the skin vessels, while PGE1 decreases skin blood flow and TEMP but increases the visceral TEMP, although SVR clearly decreases at the same rate in the two groups.

Adult↗