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PubMedDate not supplied

The alpha 2-adrenoceptor agonists clonidine, TL99 and DPI enhance vasoconstrictor responses to sympathetic nerve stimulation and noradrenaline in the rat tail artery preparation.

1. Clonidine (1-30 nmol/l) enhanced the vasoconstrictor responses to sympathetic nerve stimulation in isolated perfused artery preparations from the rat tail. Higher concentrations of clonidine produced vasoconstriction in most artery preparations and reduced the response to sympathetic nerve stimulation. 2. The enhancing effect of clonidine was not affected by prazosin but was blocked by idazoxan, indicating that it was due to activation of alpha 2-adrenoceptors. 3. The alpha 2-adrenoceptor agonists DPI and TL99, like clonidine, enhanced vasoconstrictor responses to sympathetic nerve stimulation. 4. Vasoconstrictor responses to noradrenaline were enhanced by clonidine and TL99. 5. The findings suggest that activation of postjunctional alpha 2-adrenoceptors results in facilitation of the contractile response elicited by activation of alpha 1-adrenoceptors.

Adrenergic alpha-Agonists↗

PubMed1997

Effects of magnesium sulphate on the noradrenaline-induced cerebral vasoconstrictor and pressor responses in the goat.

OBJECTIVE: To examine the ability of magnesium sulphate to counteract the noradrenaline-induced cerebral vasoconstrictor and pressor responses in goats by using both in vivo and in vitro techniques. DESIGN: Cerebral blood flow was measured in vivo by means of an electromagnetic flow probe around the internal maxillary artery. Isometric tension was recorded in vitro from rings of goat middle cerebral artery maintained in an organ bath. RESULTS: 1. In vivo. Continuous infusion of noradrenaline (10 micrograms/min) directly into the cerebral arterial supply elicited sustained decrease in cerebral blood flow (61% [SEM 3] of control values) and increase in cerebral vascular resistance (178% [SEM 9] of control values). Magnesium sulphate, injected directly into the cerebral arterial supply (10-300 mg) or infused intravenously (0.3 g and 3 g during 15 min) at the noradrenaline-induced steady state, increased cerebral blood flow by decreasing cerebral vascular resistance in a dose-dependent manner. A similar result was obtained when intravenous magnesium sulphate (3 g/15 min) was tested against the cerebral vasoconstrictor and pressor responses induced by intravenous infusion of noradrenaline (30 micrograms/min). 2. In vitro. When compared with the response obtained in a control medium (1 mmol/L Mg2+), 10 mmol/L Mg2+ significantly inhibited the maximum contraction elicited by noradrenaline (10(-8) to 3 x 10(-3) mol/L) from 45% [SEM 4] to 26% [SEM 4]. CONCLUSIONS: Magnesium sulphate reverses the noradrenaline-induced cerebral vasoconstrictor and pressor responses by a direct inhibitory action of Mg2+ on the actions of noradrenaline in the cerebral and peripheral vascular beds, which leads to a decrease in vascular resistance. These results could explain, at least in part, the beneficial effects of magnesium sulphate in the management of preeclampsia and eclampsia.

Animals↗

PubMed1981

Evidence against the involvement of prostaglandins in the vasoconstrictor action of calcium ion in rat mesenteric blood vessels.

1. Prostaglandin E2 (PGE2) has been claimed to be essential to the vasoconstrictor action of noradrenaline in rat mesenteric blood vessels. Since noradrenaline acts by releasing intracellular calcium, experiments have been performed using the perfused rat superior mesenteric artery preparation to determine whether prostaglandin synthesis is necessary for the direct vasoconstrictor action of calcium. 2. The cyclo-oxygenase inhibitors, indomethacin and 5,8,11,14-eicosatetraynoic acid (ETA), inhibited responses to noradrenaline and calcium but both were less effective in inhibiting the response to calcium than to noradrenaline. 3. PGE2 (6 ng-20 micrograms/ml) failed to overcome the inhibitory effect of indomethacin (62 micrograms/ml) and ETA (10 micrograms/ml) on the response to the EC50 of Ca2+ (100 micrograms/ml). The EC50 of Ca2+ did not significantly increase PGE2-like release by the blood vessels from the resulting value of 19 +/- 8 pg of PGE2 equivalents/min. 4. PGA1 (6 micrograms/ml) and the thromboxane A2 agonist, U-46619 (200 ng/ml), both caused full restoration of indomethacin-depressed responses to calcium, but did not restore responses depressed by ETA. U-46619 (200 ng/ml) also reversed the inhibitory effect of papaverine (4 micrograms/ml) and caused a 1.6 fold potentiation of Ca2+ responses. 5. The results do not support the hypothesis that prostaglandin synthesis is essential to the vasoconstrictor action of Ca2+ in rat mesenteric blood vessels.

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

PubMed1985

Comparison of the antagonistic effects of phentolamine on vasoconstrictor responses to exogenous and neurally released noradrenaline in vivo.

The antagonistic effects of the alpha-adrenoceptor blocking agent phentolamine on vasoconstrictor responses to intraluminal noradrenaline and lumbar sympathetic nerve stimulation were compared in the hindlimb of the anaesthetized dog. Sympathetic stimulation with 1 pulse or trains of 4-10 pulses at 0.4-40 Hz produced graded vasoconstrictor responses that were matched in amplitude by intra-arterial injections of 10(-8) - 10(-6) g noradrenaline. Phentolamine (0.5 mg kg-1 i.v.) attenuated amplitude-matched responses to both types of stimuli to quite similar extents. The extent of the effect of phentolamine on neurogenic responses was greater with 1 pulse stimulation than with trains, and greater with 4 pulse than with 10 pulse trains. The effect was maximal within 2 min of phentolamine administration and wore off in parallel with that on responses to injected noradrenaline. The results are consistent with the view that transmitter released from noradrenergic vasoconstrictor nerves acts primarily on subjunctional alpha-adrenoceptors.

Animals↗

PubMed1985

Bay K 8644, a dihydropyridine calcium agonist, augments vasoconstrictor responses to endogenous and exogenous noradrenaline in the peripheral vasculature of the dog.

The effect of Bay K 8644 (a substance known to increase calcium influx through the voltage-dependent calcium channel) on vasoconstrictor responses of resistance vessels to endogenous and exogenous noradrenaline (NA) was investigated in pentobarbitone-anaesthetized dogs which had also undergone spinal anaesthesia and bilateral vagotomy and received atropine. In these dogs the saphenous arterial bed was perfused at fixed flow rates with autologous blood to give perfusion pressure close to the systemic blood pressure. Electrical stimulation (3-30 Hz) of the saphenous nerve and single intra-arterial (i.a.) injections of noradrenaline (NA, 0.03-3 micrograms) produced an increase in perfusion pressure (vasoconstriction) in a frequency- and a dose-dependent manner, respectively. Intra-arterial infusions of Bay K 8644 (3 and 10 micrograms min-1) per se produced no significant change in perfusion pressure. However, these infusions augmented vasoconstrictor responses to both saphenous nerve stimulation (endogenous NA) and i.a. NA (exogenous NA). These results suggest that augmentation by Bay K 8644 of vasoconstrictor responses of resistance vessels to endogenous and exogenous NA is probably due to promotion of the calcium influx through calcium channels closely associated with alpha-adrenoceptors in smooth muscle cells there.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed1980

The pulmonary vasoconstrictor response to hypoxia. The hypoxia-sensitive site studied with a volatile inhibitor.

Recent investigations have revealed that a number of inhalation anesthetics, including halothane, inhibit the pulmonary vasoconstrictor response to hypoxia without affecting other vasoconstrictor stimuli. Various injectable anesthetics do not show this effect. This discrepancy could be due either to different pharmacological properties or to the different routes of administration. There is no general agreement on whether the response to hypoxia is elicited mainly by airway hypoxia or by blood hypoxemia, i.e. where within the lungs hypoxia acts. This work is an attempt to localize the hypoxia-sensitive site employing halothane. We have studied the reduction of standardized vasoconstrictor responses to hypoxia during administration of halothane via: (1) the airways, (2) the pulmonary artery and (3) the pulmonary veins (backward perfusion). Our experimental model has been two pairs of series-perfused hyperventilated isolated rat lungs. An equimolar concentration of halothane most effectively inhibits the response when presented to the alveoli, less when presented to the arterial- and least when presented to the venous segments of the pulmonary vasculature. We suggest that the response to hypoxia is inhibited by halothane at some extravascular site on the arterial side of the pulmonary vasculature, functionally closer to the alveoli than to the responding vessels. A model which combines all the data into an unifying concept has been presented.

Animals↗

PubMed1992

Vasoconstrictor reactions in spontaneously hypertensive rats versus Wistar Kyoto can be increased or decreased depending on the conditions of perfusion.

The reactions of resistance vessels in SHR and WKY hindquarters were compared during saline or blood perfusion. During saline constant-flow perfusion at all initial pressures (80-200 mmHg) sympathetic vasoconstrictor effects were greater in SHR than those in WKY. During perfusion at constant and equal pressure vasoconstrictor responses were greater in SHR vs. WKY only at high pressure--200 mmHg. On the other hand, under constant pressure conditions at lower pressures (80 and 120 mmHg) sympathetic stimulation induced weaker responses in SHR than in WKY, which at, for example, 80 mmHg was the case at every frequency of sympathetic stimulation used (2-20 Hz). Also, the responses to exogenous noradrenaline and vasopressin occurred during perfusion at low (80 mmHg) and for both equal constant-pressure conditions lower in SHR than in WKY. Comparison of sympathetic effects in SHR and WKY during blood hindquarter perfusion revealed similar results. Also, when SHR and WKY responses were compared at their ordinary levels of constant-pressure, sympathetic vasoconstrictor effects in SHR were lower than those in WKY.

Animals↗

PubMed1994

The discharge behaviour of single vasoconstrictor motoneurones in human muscle nerves.

1. The discharge behaviour of fourteen single sympathetic vasoconstrictor efferents was studied using a tungsten microelectrode inserted percutaneously into a motor fascicle of the radial or peroneal nerve in eight awake supine subjects. Units were classified as vasoconstrictor because their firing properties correlated appropriately to changes in cardiac interval and arterial pressure. 2. On average, individual vasoconstrictor units discharged in only 21% of heart beats, with an overall mean frequency of 0.47 Hz. Usually only one spike was generated per cardiac cycle. Calculated from cardiac cycles in which a unit fired from two to seven spikes, the mean within-burst firing rate was 18.8 +/- 2.5 Hz (mean +/- S.E.M.); but instantaneous frequencies above 50 Hz were occasionally observed. 3. Measured from a defined R-wave of the ECG, the spike onset latency varied over 358 +/- 33 ms, suggesting considerable variation of synaptic delays in the baroreflex arc. This latency had a relatively uniform temporal relationship with the burst onset or peak latency, compatible with a fixed recruitment order of individual sympathetic neurones. 4. In view of the low average firing rate of individual units we suggest that the variable instantaneous firing rates may optimize the contractile responses of vascular smooth muscle.

Adult↗

PubMed1987

Exaggerated postural vasoconstrictor reflex in Raynaud's phenomenon.

The central and local regulation of capillary blood flow in the finger was studied by the local xenon-133 washout technique in women with primary Raynaud's phenomenon, men with vibration induced white finger, and their respective sex matched controls. The vasoconstrictor response to venous stasis of 40 mm Hg elicited by local reflex was normal in both types of Raynaud's phenomenon. Change in posture from lying to sitting induced vasoconstriction in all groups, which was abolished by proximal nervous blockade. The vasoconstrictor response to sitting was augmented in both groups of subjects with Raynaud's phenomenon compared with their sex matched controls. These results show the existence of central and local postural vasoconstrictor reflexes in normal fingers. In both types of Raynaud's phenomenon there was hyperreactivity of the central sympathetic nervous system to orthostatic stress and normal function of digital arterioles and postganglionic sympathetic nerve fibres.

Adult↗

PubMed1979

Relationship between presence of vasoconstrictor activity in cerebrospinal fluid and time after subarachnoid haemorrhage from rupture of cerebral arterial aneurysms.

The relationship between clinical condition and vasoconstrictor factors in cerebrospinal fluid was studied in 19 patients for up to six weeks after subarachnoid haemorrhage. Vasoconstrictor activity was assayed biologically. Sixteen of 19 patients improved as vasoconstrictor activity declined; this pattern was not significantly influenced by surgery. Serial angiography was performed on three patients and a qualitative relationship was shown between arterial dilatation, clinical improvement, and reduced pharmacological activity.

Adult↗

PubMed1981

Spinal trauma: pharmacological evidence for vasoconstrictor activity in cerebrospinal fluid.

Cerebrospinal fluid from six cases of acute spinal trauma collected 0--6 days after injury was examined for vasoconstrictor activity using both human isolated cerebral arteries and animal tissues. The cerebrospinal fluid of four out of six patients was vasoactive. The identities of the vasoconstrictor substances were not established, but experiments with pharmacological antagonists showed that arterial contractions were not due to serotonin, histamine, noradrenaline, acetylcholine or angiotensin II, substances which are known potent spastic agents on cerebral arteries. Our findings would explain by the mechanism of arterial spasm, principally in the anterior spinal artery, the neuropathological appearance of central haemorrhagic necrosis in spinal cord injury. The infarction of the core of the spinal cord could be caused by vasoconstrictor substances, reported here, in the cerebrospinal fluid after spinal injury. If the identities of the substances could be established, drug therapy to prevent or relieve the spasm would be possible.

Adolescent↗

PubMed1988

Vasoconstrictor response to cold in forestry workers: a prospective study.

In a five year prospective study of the vasoconstrictor response to cold 37 forestry workers were investigated in 1978 and again in 1983. The subjects were classified into three groups: group A (n = 13): no subjective finger symptoms in 1978 and continued sawing until 1983; group B (n = 12): no symptoms in 1978 and stopped sawing before 1983; group C (n = 12): vibration induced white finger (VWF) in 1978. A cold provocation test measuring the finger systolic blood pressure with a cuff and strain gauge technique during combined body cooling and finger cooling to 30 degrees, 15 degrees, and 6 degrees C was applied to all subjects at both investigations. In 1978 all groups had an increased cold response when compared with that of 20 non-exposed controls (p less than 0.05), and the response was more exaggerated in group C than in groups A and B (p less than 0.01). From 1978 to 1983 the vasoconstrictor response increased in group A (p less than 0.05), was in group B (p greater than 0.10), and improved in group C (p less than 0.05). The changes in cold response in groups A and C were significantly larger than the within day variation of the method (p less than 0.01). The aggravation of group A indicates that a further five years use of anti-vibration chain saws induced an increased hyperreactivity in the vasoconstrictor mechanisms but led to subjective symptoms of VWF in only one subject. The improvement in group C was in accordance with the improvements of subjective finger symptoms and was associated with a previous shift from saws without vibration damping devices to anti-vibration saws and with cessation of work. The results of group C indicate that VWF may improve or subjectively disappear if exposure to vibration is reduced or stopped. The cold provocation test was more sensitive than the Taylor-Pelmear stage assessments (p<0.05). The test may be of guidance in evaluation preventive measures.

Adolescent↗

PubMed2002

Effects of aging on vasoconstrictor and mechanical properties of rat skeletal muscle arterioles.

Exercise capacity and skeletal muscle blood flow during exercise are reduced with advancing age. This reduction in blood flow capacity may be related to increased reactivity of skeletal muscle resistance vessels to vasoconstrictor stimuli. The purpose of this study was to test the hypothesis that aging results in increased vasoconstrictor responses of skeletal muscle resistance arterioles. First-order (1A) arterioles (90-220 microm) from the gastrocnemius and soleus muscles of young (4 mo) and aged (24 mo) Fischer-344 rats were isolated, cannulated, and pressurized via hydrostatic reservoirs. Vasoconstriction in response to increases in norepinephrine (NE; 1 x 10(-9)-1 x 10(-4) M) and KCl (20-100 mM) concentrations and increases in intraluminal pressure (10-130 cmH(2)O) were evaluated in the absence of flow. Responses to NE and KCl were similar in both soleus and gastrocnemius muscle arterioles from young and aged rats. In contrast, active myogenic responses to changes in intraluminal pressure were diminished in soleus and gastrocnemius arterioles from aged rats. To assess whether alterations in the mechanical properties of resistance arterioles underlie altered myogenic responsiveness, passive diameter responses to pressure and mechanical stiffness were evaluated. There was no effect of age on the structural behavior (passive pressure-diameter relationship) or stiffness of arterioles from either the soleus or gastrocnemius muscles. These results suggest that aging does not result in a nonspecific decrease in vasoconstrictor responsiveness of skeletal muscle arterioles. Rather, aging-induced adaptations of vasoreactivity of resistance arterioles appear to be limited to mechanisms that are uniquely involved in the signaling of the myogenic response.

Aging↗

PubMed1987

Vasoconstrictor role for vasopressin in conscious, sodium-depleted rats.

To define the role of vasopressin as a vasoconstrictor hormone in sodium depletion, systemic hemodynamics and regional blood flow distribution were examined in conscious Sprague-Dawley rats after 6 days of a low-sodium diet. Studies were performed after selective or combined blockade with the vasopressin antagonist [d(CH2)5Tyr(Me)]AVP (AVPA), enalaprilat (CEI), and phentolamine (PHENTOL). Plasma levels of vasopressin were increased significantly after CEI and increased further after PHENTOL and CEI plus PHENTOL. AVPA had no effect on blood pressure, whether given alone or in the presence of PHENTOL, CEI, or CEI plus PHENTOL. Significant falls in peripheral vascular resistance associated with reflex increases in cardiac output were observed when AVPA was given to animals pretreated with either CEI or PHENTOL but not both. AVPA alone produced no significant changes in regional blood flow distribution, but a vasoconstrictor action of vasopressin in the renal vascular bed was revealed after prior treatment with CEI or PHENTOL. Muscle blood flow was also increased in the PHENTOL plus AVPA group compared with the PHENTOL group. No significant additional effects of AVPA were revealed by pretreatment with CEI, PHENTOL, or CEI plus PHENTOL for mesenteric, hepatic, splenic, or cerebral vascular beds. It is suggested that vasopressin acts as a vasoconstrictor hormone in conscious sodium-depleted rats when either the renin-angiotensin system or alpha-adrenergic system is inhibited but not when both systems are blocked. The renal vascular bed is an important site for vasopressin-induced vasoconstriction under these circumstances.

Adaptation, Physiological↗

PubMed1987

Age-related changes in adrenergic vasoconstrictor responses of the rat hindlimb.

Vascular adrenergic responses were examined in the hindlimb perfused with blood at constant flow using pentobarbital-anesthetized male Fischer 344 rats aged 6, 12, 20, and 24 mo. The increase in hindlimb perfusion pressure to lumbar sympathetic nerve stimulation was significantly smaller in 20- and 24-mo-old rats than in younger animals, whereas vasoconstrictor responses to intraarterial administration of norepinephrine, L-phenylephrine, and methoxamine were reduced only in the 24-mo-old animals. Thus neurogenic vasoconstriction in the hindlimb is reduced at 20 mo of age, whereas there is a more generalized postjunctional loss of adrenergic responsiveness at 24 mo. In the presence of the beta-adrenoceptor antagonist, propranolol, vasoconstrictor responses to exogenous norepinephrine did not differ when 12- and 20-mo-old animals were compared. Furthermore, in the presence of propranolol the nerve-mediated rise in hindlimb perfusion pressure also did not differ in 12- and 20-mo-old rats. Blockade of neuronal norepinephrine uptake with cocaine produced a greater potentiation of vasoconstrictor responses to both nerve stimulation and exogenous norepinephrine in the older rats. Therefore, the reduced nerve-mediated vasoconstriction in 20-mo-old rats may be due to neuronal activation of beta-adrenoceptors as well as enhanced neuronal norepinephrine reuptake.

Adrenergic Fibers↗

PubMed1985

Mechanism of action of vasoconstrictor responses to atriopeptin II in conscious SHR.

Previous studies have demonstrated that infusion of synthetic atriopeptin II (AP II) lowered arterial pressure, reduced regional blood flow, and increased total peripheral and regional vascular resistances in conscious spontaneously hypertensive rats (SHR). This study was designed to examine the mechanism(s) involved in regional vasoconstrictor responses to AP II. In these experiments, hemodynamic actions of AP II were examined in control, 6-hydroxydopamine-treated (chemically sympathectomized), and renal-denervated groups of instrumented conscious SHR. Infusion of AP II (1 microgram X kg-1 X min-1) caused similar reductions in mean arterial pressure in control (-22 +/- 2 mmHg), chemically sympathectomized (-23 +/- 2 mmHg), and renal-denervated (-23 +/- 3 mmHg) SHR. In control SHR, AP II infusion reduced renal (-20 +/- 3%), mesenteric (-26 +/- 2%), and hindquarters (-18 +/- 10%) blood flow and increased regional vascular resistance in all three beds. Chemical sympathectomy prevented the fall in renal blood flow (RBF) and significantly abolished the regional vasoconstrictor responses to AP II infusion. In unilateral renal-denervated groups of SHR, AP II reduced renal vascular resistance (RVR) -11 +/- 3% but failed to alter RBF (-3 +/- 1%) in denervated kidneys. In contrast, RVR increased (20 +/- 7%) and RBF was significantly reduced (-29 +/- 3%) in contralateral-innervated kidneys. This study demonstrated that chemical or surgical destruction of renal sympathetic nerves abolished AP II-induced increases in RVR. These data further indicate that in conscious SHR the regional vasoconstrictor responses to AP II infusion appear to be mediated by increases in sympathetic tone rather than through direct vascular actions of AP II.

Animals↗

PubMed2001

Diurnal variation in cutaneous vasodilator and vasoconstrictor systems during heat stress.

It is not clear whether the diurnal variation in the cutaneous circulatory response to heat stress is via the noradrenergic vasoconstrictor system or the nonadrenergic active vasodilator system. We conducted whole body heating experiments in eight male subjects at 0630 (AM) and 1630 (PM). Skin blood flow was monitored by laser-Doppler flowmetry at control sites and at sites pretreated with bretylium (BT) to block noradrenergic vasoconstriction. Noninvasive blood pressure was used to calculate cutaneous vascular conductance. The sublingual temperature (T(or)) threshold for cutaneous vasodilation was significantly higher in PM at control and at BT-treated sites (both P < 0.01), suggesting the diurnal shift in threshold depends on the active vasodilator system. The slope of cutaneous vascular conductance as a percentage of its maximum with respect to T(or) was significantly lower in AM at control sites only. Also, in the AM, the slope at control sites was significantly lower than that at BT-treated sites (P < 0.05), suggesting that the diurnal change in the sensitivity of cutaneous vasodilation depends on vasoconstrictor system function. Overall, the diurnal variation in the reflex control of skin blood flow during heat stress involves both vasoconstrictor and active vasodilator systems.

Anti-Arrhythmia Agents↗

PubMed1998

Vasoconstrictor responses of coronary resistance arteries in exercise-trained pigs.

Coronary resistance arteries isolated from exercise-trained pigs have been shown to exhibit enhanced myogenic reactivity (J. M. Muller, P. R. Myers, and M. Harold Laughlin. J. Appl. Physiol. 75: 2677-2682, 1993). The purpose of this study was to test the hypothesis that exercise training results in enhanced vasoconstrictor responses of these arteries to all vasoconstrictor stimuli [specifically acetylcholine (ACh), endothelin-1 (ET-1), KCl, and the Ca2+ channel-agonist Bay K 8644]. Female Yucatan miniature swine were trained (Trn) on a motor-driven treadmill (n = 16) or remained sedentary (Sed, n = 15) for 16-20 wk. Arteries 50-120 micron in diameter were isolated and cannulated with micropipettes, and intraluminal pressure was set at 60 cmH2O throughout experiments. Vasoreactivity was evaluated by examining constrictor responses to increasing concentrations of ACh (10(-9) to 10(-4) M), ET-1 (10(-10) to 10(-8) M), KCl (bath replacement with isotonic physiological saline solution containing 30 or 80 mM), and Bay K 8644 (10(-9) to 10(-6) M). Constricted diameters are expressed relative to the passive diameter observed after 100 microM SNP. All four constrictors produced similar decreases in diameter in arteries from both groups [ACh: 0.52 +/- 0.07 (Trn) and 0.54 +/- 0,06 (Sed); ET-1: 0.66 +/- 0.05 (Trn) and 0.70 +/- 0.07 (Sed); KCl: 0.66 +/- 0.05 (Trn) and 0.70 +/- 0.07 (Sed); Bay K 8644: 0.86 +/- 0.05 (Trn) and 0. 76 +/- 0.05 (Sed)]. Present results combined with previous observations indicate that exercise training does not alter vasoconstrictor responses of porcine coronary resistance arteries but specifically increases myogenic reactivity. Thus the underlying cellular mechanisms for myogenic tone are altered by training but not receptor-mediated mechanisms (ACh and ET-1) nor voltage-gated Ca2+ channels (KCl and Bay K 8644) in coronary resistance arteries.

Acetylcholine↗