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PubMed1981

Influence of prostaglandins on vasoconstrictor responses in the hindquarters vascular bed of the cat.

The effects of prostaglandins (PG), A1, A2, B2, E1, 6-keto-E1, F2 alpha and indomethacin on vascular resistance and vasoconstrictor responses were investigated in the feline hindquarters vascular bed under conditions of controlled flow so that changes in perfusion pressure directly reflect changes in vascular resistance. Infusion of PGE1, PGE2 and 6-keto-PGE1 (3 microgram/min) into the abdominal aorta significantly dilated the hindquarters vascular bed and inhibited vasoconstrictor responses to sympathetic nerve stimulation and intra-arterial injections of angiotensin, whereas hindquarters vasoconstrictor responses to tyramine and exogenous norepinephrine were unaffected. Infusion of PGA1, A2, B2 and F2 alpha at a similar rate produced transient changes in hindquarters vascular resistance and did not consistently alter vasoconstrictor responses to sympathetic nerve stimulation, angiotensin, norepinephrine and tyramine. Indomethacin in a dose which greatly attenuates the response to intravenous administration of arachidonic acid enhanced responses to nerve stimulation and norepinephrine. In addition, indomethacin had little or no effect on hindquarters perfusion pressure and systemic arterial pressure. These data suggest that E series prostaglandins possess the ability to modulate the actions of the sympathetic nervous system and angiotensin in the feline hindquarters vascular bed. In addition, these data suggest that PGEs, upon enzymatic conversion and dehydration to A and B series prostaglandins, lose their ability to consistently affect vasoconstrictor responses. Experiments with indomethacin further suggest that locally formed prostaglandins do modulate the effects of the sympathetic nervous system of the feline hindquarters.

Angiotensin II↗

PubMed1982

Transmission of impulses from pre- to postganglionic vasoconstrictor and sudomotor neurons.

Transmission of impulses of pre- to postganglionic neurons supplying skeletal muscle and skin of the cat's hindlimb and tail was investigated. The objective of the study was to determine whether these postganglionic neurons can be influenced from the preganglionic side by non-nicotinic synaptic mechanisms in the lumbar sympathetic chain ganglia. The activity of the postganglionic neurons was recorded from their axons being isolated from peripheral skin and muscle nerves. (1) Vasoconstrictor neurons can be activated by muscarinic action of released acetylcholine and by a non-cholinergic synaptic mechanism. This type of non-nicotinic excitation of postganglionic vasoconstrictor neurons requires the activation of thin, probably unmyelinated preganglionic axons and considerable summation. Postganglionic sudomotor and pilomotor neurons cannot be activated in this way. (2) Ongoing activity in postganglionic vasoconstrictor neurons, but not in sudomotor neurons, can be enhanced for up to 60 min by brief trains of stimuli applied to the preganglionic site. Also this enhancement requires the activation of thin preganglionic axons. (3) Stimulation of thin preganglionic axons leads to an activation of muscle vasoconstrictor neurons via non-nicotinic synaptic mechanisms in the ganglia after complete block of nicotine transmission. (4) Postganglionic vasoconstrictor neurons and sudomotor neurons may be inhibited by a catecholaminergic autogenic mechanism in the ganglia. (5) The results indicate that integration may take place in the sympathetic chain ganglia by other than divergent and convergent processes. In this integration muscarinic actions of released acetylcholine and non-cholinergic synaptic mechanisms may be involved.

Acetylcholine↗

PubMed1993

Quantitative vasoconstrictor assay for topical corticosteroids: the puzzling case of fluocinolone acetonide.

BACKGROUND: The validity of the vasoconstrictor test has been questioned because of the apparent nonequivalence of some generic corticosteroid products. OBJECTIVE: Our purpose was to determine the vasoconstrictor activity of a generic 0.025% fluocinolone acetonide ointment by two different methods, dilution by volume and dilution by area of application. METHODS: Vasoconstrictor activity on a visual 4-point scale was measured in 20 volunteers. Topical fluocinolone acetonide ointment (0.025%) was tested by comparing dilution by volume (1:1, 1:3, and 1:7) in petrolatum and dilution by area of application. Fluocinolone release from the diluted ointments was also measured with an in vitro method. RESULTS: Dilution by area gave the expected results, a decreasing average vasoconstrictor score; but dilution by volume did not. Both the 1:1 and 1:3 dilutions inexplicably showed greater activity than the full-strength product; this finding was similarly reflected in the in vitro studies that showed a greater rate of drug release from the 1:1 and 1:3 dilutions. CONCLUSION: Dilution by area provides a useful quantitative assay for comparative vasoconstrictor activity.

Adult↗

PubMed1996

Sympathetic vasoconstrictor neurons projecting from the guinea-pig superior cervical ganglion to cutaneous or skeletal muscle vascular beds can be distinguished by soma size.

We have used a combination of retrograde axonal tracing and intracellular dye injections to determine the soma size of sympathetic vasoconstrictor neurons projecting from the superior cervical ganglion to the cutaneous vascular bed of the eartips, or to the vascular beds of the masseter muscle, of guinea-pigs. Neurons projecting to vasculature of the masseter muscle had a cross-sectional area of 956 +/- 295 microns2 (mean +/- SD; n = 45 cells) and were significantly larger than neurons projecting to the vasculature of the eartip skin (mean cross-sectional area +/- SD, 604 +/- 251 microns2; n = 39 cells). These results are consistent with physiological observations showing that muscle vasoconstrictor neurons have faster conduction velocities than cutaneous vasoconstrictor neurons. Furthermore, they suggest that muscle vasoconstrictor neurons may innervate a larger volume of vasculature compared with cutaneous vasoconstrictor neurons.

Animals↗

PubMed1992

Vasoconstrictor, vasodilator and pilomotor pathways in sympathetic ganglia of guinea-pigs.

Triple-labelling immunofluorescence and retrograde axonal tracing with fluorescent dyes have been combined to identify and characterize the neuropeptide content of vasoconstrictor, vasodilator and pilomotor neurons in the lumbar sympathetic ganglia of guinea-pigs. Postganglionic noradrenergic pilomotor neurons lacked immunoreactivity to neuropeptide Y and comprised up to about 30% of postganglionic neurons. Most post-ganglionic noradrenergic neurons that contained neuropeptide Y immunoreactivity were likely to be vasoconstrictor neurons, although some noradrenergic neurons containing neuropeptide Y projected to pelvic viscera. Vasoconstrictor neurons comprised up to about 60% of postganglionic neurons. About 15% of postganglionic neurons were non-noradrenergic and contained immunoreactivity to vasoactive intestinal peptide, neuropeptide Y and dynorphin. They mostly innervated blood vessels supplying skeletal muscles and were likely to be vasodilator neurons. Endings of presumed preganglionic neurons containing immunoreactivity to substance P were exclusively associated with vasodilator neurons. Conversely, presumed preganglionic endings containing immunoreactivity to calcitonin gene-related peptide were exclusively associated with vasoconstrictor neurons, although not all vasoconstrictor neurons had such endings associated with them. Presumed preganglionic terminals containing immunoreactivity to enkephalin were associated with some postganglionic neurons in each functional class. These results show that preganglionic and postganglionic sympathetic neurons lying in different functional pathways can be distinguished by their neuropeptide content as well as their projections. The identification of neurochemically distinct functional pathways begins to explain how the sympathetic nervous system is organized to allow the precise control of discrete target tissues.

Animals↗

PubMed1996

Dendritic morphology of presumptive vasoconstrictor and pilomotor neurons and their relations with neuropeptide-containing preganglionic fibres in lumbar sympathetic ganglia of guinea-pigs.

We have used intracellular dye-filling combined with multiple-labelling immunofluorescence to examine the dendritic morphology of neurons and their relations with neuropeptide-containing preganglionic terminals in the lumbar sympathetic chain of guinea-pigs. Presumptive vasoconstrictor neurons with immunoreactivity for both tyrosine hydroxylase and neuropeptide Y dendritic fields that were significantly smaller, on average, than those of presumptive pilomotor neurons containing immunoreactivity to tyrosine hydroxylase but not to neuropeptide Y. However, there was considerable variation in the sizes of the dendritic fields of the vasoconstrictor neurons. Preganglionic nerve terminals containing immunoreactivity to calcitonin gene-related peptide, but not to substance P, only surrounded cell bodies of vasoconstrictor neurons containing immunoreactivity to tyrosine hydroxylase and neuropeptide Y. In most cases, the neuropeptide-containing preganglionic terminals were not associated closely with the distal dendrites of these neurons. Few neuropeptide-containing terminals were associated closely with either the cell bodies or dendrites of the pilomotor neurons. These results show that there is a considerable range in the size of dendritic trees of sympathetic final motor neurons. Some of this variation is related to the pathways within which the neurons lie, so that presumptive pilomotor neurons generally are larger than presumptive vasoconstrictor neurons. The marked variation in size of vasoconstrictor neurons raises the possibility that there may be a size dependent recruitment of these neurons, similar to that seen in pools of spinal motor neurons. The distribution of the peptide-containing preganglionic endings suggests that they would act predominantly at the cell body and proximal dendrites of the final motor neurons.

Animals↗

PubMed1997

The recruitment pattern of single vasoconstrictor neurons in human.

The aim of this study is to determine the recruitment pattern among individual vasoconstrictor neurons under the baroreceptor-mediated influence in man. Spikes of single vasoconstrictor units were detected from microneurograms with a template-matching method. A total of 39 single vasoconstrictor units were detected. Single vasoconstrictor units were different from each other in their susceptibility to be activated in response to changes in the R-R interval or blood pressure. The units with higher firing probability had a shorter threshold R-R interval and a higher threshold diastolic blood pressure than units with lower firing probability. In sympathetic responses consisting of only one spike (single-spike responses), units with a lower threshold frequently appeared and units with a higher threshold joined mull-spike responses. The units with a short threshold R-R interval tended to have a long inhibitory latency from R wave, suggesting low conduction velocity. The correlation between firing probability and firing threshold and that between appearance in single-spike response and multi-spike response suggest a hierarchical manner of recruitment of vasoconstrictor units. For beat-to-beat responses, however, some deviation from the hierarchical recruitment was also observed.

Adult↗

PubMed1999

NPY Y2 receptor agonist, N-acetyl [Leu28,Leu31]NPY24-36, reduces renal vasoconstrictor activity in anaesthetised dogs.

The actions of neuropeptide Y (NPY) at the autonomic neuroeffector junction have been attributed to two main receptor subtypes. At NPY Y1 receptors, located postsynaptically, NPY has been shown to produce vasoconstriction, or to potentiate the action of other vasoconstrictor agents. At NPY Y2 receptors, located presynaptically on nerve terminals, NPY inhibits the release of neurotransmitter from autonomic nerve terminals. In these experiments we have used the specific NPY Y2 receptor agonist, N-acetyl [Leu28,Leu31]NPY, which lacks local constrictor activity, and have demonstrated inhibition of nerve-evoked vasoconstriction in the renal circulation of anaesthetised dogs in a way that suggests an intra-renal regional specificity. Under control conditions stimulation of the renal sympathetic nerves over a range of frequencies (1-5 Hz) reduced renal vascular conductance and glomerular filtration rate (GFR). Following the injection of the selective NPY Y2 receptor agonist, N-acetyl [Leu28,Leu31]NPY24-36, nerve-evoked reductions in renal conductance were reduced by over 45%. At the lowest stimulation frequencies, reduced vasoconstrictor activity was associated with a marked increase in GFR in the presence N-acetyl [Leu28,Leu31]NPY24-36. At both higher levels of stimulation N-acetyl [Leu28,Leu31]NPY24-36 significantly inhibited vasoconstrictor activity and attenuated the nerve-evoked reductions in GFR. Full recovery of both variables was observed 20 min after N-acetyl [Leu28,Leu31]NPY24-36 injection. N-acetyl [Leu28,Leu31]NPY24-36 produced a similar inhibition of renal vasoconstrictor activity when the renal nerves were left intact and activated reflexly. These results suggest that NPY can act via NPY Y2 receptors to inhibit sympathetic vasoconstrictor activity in the renal circulation of dogs. On the basis of the demonstrated dissociation of effects on vascular conductance and GFR, we suggest that this might result from a preferential action of the NPY Y2 agonist on sympathetic nerves supplying the afferent arteriole of the kidney.

Anesthesia↗

PubMed1998

Sympathetic vasoconstrictor reflex pattern in patients with complex regional pain syndrome.

Twenty patients suffering from complex regional pain syndrome (CRPS) and 21 healthy control subjects were examined to evaluate sympathetic reflex vasoconstriction. The mean age of the 12 female and eight male patients was 48.9 (21-72) years. At the time of investigation the median duration of the disease was 8.5 weeks (2-70). Twenty-one healthy subjects were investigated for control. Different maneuvers, such as the veno-arteriolar reflex (VAR), inspiratory gasp (IG), cold pressor test (CP) and mental arithmetic (MA), were employed to induce vasoconstriction while the cutaneous blood flow of the affected and the contralateral limb was recorded. In addition, the skin temperature of both limbs was measured by infrared thermography. In 14 of 20 patients and in 14 of 21 control subjects vasoconstriction due to the provocation tests could be measured, while the remaining six patients and seven controls showed vasodilatation in at least one test, and by that they were excluded from analysis of vasoconstrictor reflex pattern. After thermoregulatory adaptation skin temperature was not different between the affected and the unaffected limb. Sympathetic reflex vasoconstriction triggered by MA which represents cortical generated, moderate vasoconstrictor stimulus, was significantly reduced on the affected limb (102.9% of prestimulus period) when compared to the control limb (85.0%, P < 0.002) or to controls (84.8%, P < 0.001). VAR (pure postganglionic), IG and CP (both spinal and supraspinal), representing stronger vasoconstrictor stimuli, revealed no significant side to side difference of sympathetic vasoconstriction and no significant difference as compared to controls. In conclusion our findings prove impairment of sympathetic vasoconstrictor activity after central vasoconstrictor stimulation in CRPS, and possible mechanisms are discussed.

Adult↗

PubMed2000

Effects of a nitrate-free interval on tolerance, vasoconstrictor sensitivity and vascular superoxide production.

OBJECTIVES: In the present study, we tested whether a nitrate-free interval is able to prevent increases in vascular superoxide (O2*-) and the development of hypersensitivity to vasoconstrictors and whether this may result in restoration of vascular nitroglycerin (NTG) sensitivity. BACKGROUND: Intermittent NTG-patch treatment (12 h patch on/patch-off) has been shown to increase ischemic periods in patients with stable coronary arteries, suggesting a rebound-like situation during the patch-off period. Recently, we demonstrated that long-term treatment with NTG induces tolerance, which was in part related to increases in vascular O2*- and increased vasoconstrictor sensitivity. METHODS: New Zealand white rabbits received a continuous application of NTG patches (0.4 mg/h) or an intermittent application of NTG patches (12 h patch on, 12 h patch off) for three days. Isometric tension studies were performed with aortic rings, and vascular O2*- was estimated using lucigenin-derived chemiluminescence (5 micromol/liter). Expression of the copper/zinc (Cu/Zn) superoxide dismutase (SOD) was assessed by Western blotting, and SOD activity was measured by autooxidation of 6-hydroxydopamine. RESULTS: Continuous treatment with NTG caused tolerance to NTG, cross-tolerance to the endothelium-dependent vasodilator acetylcholine, increased vascular O2*-, reduced Cu/Zn SOD expression and increased sensitivity to vasoconstrictors such as phenylephrine, serotonin and angiotensin II. On/off treatment with NTG improved tolerance, corrected endothelial dysfunction and decreased vascular O2*-. In addition the reduction in SOD expression was less pronounced, whereas increases in the sensitivity to vasoconstrictors such as phenylephrine and serotonin remained nearly unchanged. CONCLUSIONS: Enhanced vasoconstrictor sensitivity may explain, at least in part, the rebound phenomena observed in patients during a 12-h NTG patch-off period.

Acetylcholine↗

PubMed1989

Conjunctival goblet cell response to vasoconstrictor use.

Vasoconstrictors such as phenylephrine and naphazoline are used in ophthalmology to decrease hyperemia associated with allergic conjunctivitis and contact lens wear. There is a suspicion, however, that chronic use of these agents can produce dry-eye symptoms in some patients. The purpose of this study was to determine whether vasoconstrictor use interferes with tear film adequacy by decreasing mucin-secreting goblet cells. Cellulose acetate filter strip impressions were taken from the bulbar conjunctiva of rabbit eyes treated with vasoconstrictors or artificial tears for varying periods of time, and the number of goblet cells per light microscopic field counted. There was no significant difference between the number of goblet cells in control and vasoconstrictor-treated animals within each time period. These results indicate that conjunctival goblet cell density is not significantly affected by topical vasoconstrictor use.

Administration, Topical↗

PubMed1991

Role of the endothelium in modulation of the acetylcholine vasoconstrictor response in porcine coronary microvessels.

STUDY OBJECTIVE: The aim was to investigate the role of the endothelium in modulating the acetylcholine response in porcine coronary microvessels and compare the results with simultaneously studied large coronary arteries. DESIGN: Coronary microvessels [104 (SEM 3.3) microns; range 38-150] were removed from fresh porcine hearts and studied in vitro during no flow constant pressure conditions. Endothelium derived relaxing factor (EDRF) activity and the role of the endothelium in modulating the acetylcholine response in microvessels was assessed by measuring changes in intraluminal diameter using a video tracking device. Large coronary arteries were simultaneously studied using conventional isometric ring techniques. EXPERIMENTAL MATERIAL: Fresh porcine hearts were obtained from a local slaughterhouse. MEASUREMENTS AND MAIN RESULTS: Acetylcholine was a potent vasoconstrictor (EC50 = 0.17 microM) of passively distended microvessels. The effects of EDRF were studied by either inactivation with haemoglobin or inhibition of EDRF synthesis with N-omega-nitro-L-arginine. Preconstricted microvessels exposed to either N-omega-nitro-L-arginine or haemoglobin constricted further, consistent with basal release of EDRF. Neither drug affected passively distended microvessels. The acetylcholine vasoconstrictor response was potentiated after exposure of microvessels to either drug. Atropine, but not indomethacin, blocked the acetylcholine response in microvessels. As with microvessels, acetylcholine was a vasoconstrictor (EC50 = 0.3 microM) of large coronary arteries. In contrast to microvessels, indomethacin antagonised acetylcholine vasoconstriction in vessels with intact endothelium. Bioassay experiments using indomethacin-treated large epicardial donor artery segments showed basal release of EDRF but no EDRF release in response to acetylcholine. CONCLUSIONS: The results show the microvessels and large coronary arteries are similar in their vasoconstrictor response to acetylcholine, that both release EDRF basally, and that vasoconstriction to acetylcholine is importantly modulated by the endothelium. In large arteries, acetylcholine does not stimulate EDRF release and, in contrast to microvessels, a cyclo-oxygenase product influences the vasoconstrictor action of acetylcholine.

Acetylcholine↗

PubMed1982

Changes after arterial reconstruction in the forefoot local vasoconstrictor response to increased venous transmural pressure.

Local blood flow regulation on the forefoot was studied by the 133Xe wash-out technique in twenty-seven patients before and after arterial reconstruction for occlusive arterial disease. In thirteen limbs with severe symptoms the local vasoconstrictor response to increased venous pressure was absent preoperatively, as blood flow in the foot increased in median by 47% when the foot was lowered 40 cm below the heart. Three months postoperatively the vasoconstrictor response had returned as blood flow decreased 28% during lowering. Fourteen limbs with milder symptoms had a vasoconstrictor response before operation. In nine limbs of this group treated with aortoiliac reconstruction the vasoconstrictor response was absent at the early postoperative examination, but the response returned till the late examination. It is concluded that the local vasoconstrictor response is normalized after arterial reconstruction. Disturbances may, however, occur in the postoperative period, possibly due to operative stress.

Adult↗

PubMed1991

Differential actions of platelet-activating factor (PAF) receptor antagonists on the vasodilator and vasoconstrictor effects of PAF in the rat perfused heart.

Selectivity for blocking the coronary vasodilator and vasoconstrictor effects of platelet-activating factor (PAF) in the rat perfused heart was observed with different PAF antagonists. CV-6209 showed selectivity for blocking the vasodilator effect of PAF and a higher concentration (10 fold) was required to block the vasoconstrictor effect. The remaining PAF antagonists (FR-900452, WEB 2086 and BN-50739) showed selectivity for blocking the vasoconstrictor effect of PAF (10, 200 and 1000 fold respectively). A combination of low concentrations of CV-6209 (10 nM) with FR-900452 (5 microM) or WEB 2086 (0.5 microM) was effective in blocking both the vasodilator and vasoconstrictor effects of PAF. CV-6209 and WEB 2086 did not affect the vasodilator action of leukotriene B4 (LTB4) and the vasoconstrictor action of LTC4 and LTD4. Our results support the hypothesis that the functionally opposite effects of PAF in the rat perfused heart may be mediated by different PAF receptor subtypes.

Animals↗

PubMed1980

Thermoregulatory and rhythm-generating mechanisms governing the sudomotor and vasoconstrictor outflow in human cutaneous nerves.

1. Recordings of multiunit sympathetic activity were made from human nerve fascicles supplying hairy and glabrous skin of the extremities in healthy subjects exposed to different ambient temperatures. Sudomotor and vasomotor events accompanying the neural activity were monitored by simultaneous recordings of electrodermal and pulse plethysmographic events (Pleth) in the neural innervation zones. 2. By exposing the subject to warm (43 degrees C) or cold (15 degrees C) environments, it was possible to obtain a selective activation of either the sudomotor or the vasoconstrictor neural system, respectively, with suppression of spontaneous activity in the other system. 3. Bursts of both vasoconstrictor and sudomotor nerve activity were found to occur at certain preferred intervals which were integer multiples of a period of about 0 . 6 sec (100 cycles/min). With high sudomotor or vasoconstrictor tone the 100 cycles/min rhythm was prominent but with decreasing tone slower subharmonic rhythms prevailed. Respiratory rhythms were also discerned as well as slower rhythms attributable to oscillatory tendencies in thermoregulatory servos. 4. Vasoconstrictor bursts had longer mean duration than sudomotor bursts, a finding attributed to a slower conduction velocity of vasoconstrictor as compared to sudomotor impulses. 5. With increasing incidence of bursts transient electrodermal or plethysmographic responses following individual bursts merged, and thus the fast neural rhythms were not discernible in either the electrodermal or Pleth traces. Given increments in firing rate of nerves produced less additional vasoconstriction at high than at low firing rates. The rhythm generating mechanisms may help to restrict rates of individual fibres to the low range which provides high gain in the neuroeffector transfer functions.

Action Potentials↗

PubMed1985

Sympathetic and local vasoconstrictor response to cold in vibration induced white finger.

To study the relative roles of sympathetic and local vasoconstrictor response to cold in vibration induced white finger (VWF) seven lumberjacks with bilateral VWF and seven age matched controls were investigated. During body cooling finger systolic blood pressure was measured with a cuff technique simultaneously on one affected finger on each hand at 30 degrees, 15 degrees, and 6 degrees C. Both affected fingers had an increased vasoconstrictor response at 15 degrees and 6 degrees C compared with the control group (p less than or equal to 0.05). During unilateral sympathetic nerve block the cold provocation test was repeated on both fingers. The unblocked finger affected by VWF showed no significant difference in the cold response between the two cold provocation tests (p greater than 0.10). The local cold response of blocked finger did not differ from that of the control group (p greater than 0.10). The sympathetic vasoconstrictor response to cold was estimated as the difference between the cold response before nerve block and the cold response during nerve block. The median sympathetic vasoconstrictor response at 6 degrees C was about twice as large as the local response during nerve block (p less than 0.05). The results indicate that the sympathetic vasoconstrictor response to cold plays the dominant part in VWF.

Aged↗

PubMed1987

Influence of nisoldipine on vascular resistance and vasoconstrictor responses in cats.

The influence of nisoldipine, a calcium entry antagonist, on vascular resistance and vasoconstrictor responses was investigated in the anesthetized cat. Nisoldipine, a dihydropyridine calcium entry blocking agent, decreased total peripheral resistance and dilated the intestinal vascular bed. This calcium antagonist blocked intestinal vasoconstrictor responses to BAY K 8644, a nifedipine analogue, which promotes calcium entry. The calcium entry antagonist decreased intestinal vasoconstrictor responses to sympathetic nerve stimulation, norepinephrine, and tyramine. Nisoldipine also reduced intestinal vasoconstrictor responses to potassium chloride and agonists that elicit vasoconstriction by specific receptor-mediated actions including stimulation of alpha 1- and alpha 2-adrenoceptors. The vasodilator and inhibitory effects of nisoldipine on vasoconstrictor responses were reversible, and responses returned to control value over a 60-min period. The present data suggest that an extracellular source of calcium is required for maintenance of tone and for vasoconstriction induced by neuronally released or exogenous norepinephrine as well as a diverse group of agents that act through specific receptor mechanisms or depolarize vascular smooth muscle. The present results suggest that similar sources of calcium are required for vasoconstriction elicited by alpha 1- and alpha 2-adrenoceptor agonists in the feline intestinal vascular bed.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed1989

Nisoldipine inhibits vasoconstrictor responses in the cat pulmonary vascular bed.

The influence of nisoldipine, a dihydropyridine calcium entry antagonist, on vascular resistance and vasoconstrictor responses was investigated in the feline pulmonary vascular bed under conditions of controlled blood flow. The calcium channel blocking agent caused a small reduction in lobar vascular resistance and blocked pulmonary vasoconstrictor responses to BAY K 8644, an agent which promotes calcium entry. The calcium entry blocking agent also reduced pulmonary vasoconstrictor responses to methoxamine and to BHT 933, alpha 1- and alpha 2-adrenoceptor agonists, and to U 46619, an agent which mimics the actions of thromboxane A2. Although there was a marked difference in vasoconstrictor potency in the pulmonary vascular bed, responses to the thromboxane mimic and to the alpha 1- and alpha 2-adrenoceptor agonists were reduced by approximately the same extent. The increases in systemic arterial pressure in response to BAY K 8644, methoxamine, and BHT 933 were also reduced by nisoldipine, and the calcium entry antagonist reduced systemic arterial pressure and systemic vascular resistance. The results of the present study suggest that an extracellular source of calcium is required for the maintenance of vascular tone and for the expression of vasoconstrictor responses, resulting from activation of alpha 1- and postjunctional alpha 2-adrenoceptors and thromboxane receptors in the feline pulmonary vascular bed.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗