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PubMed2006

Anal electrical stimulation with long pulses increases anal sphincter pressure in conscious dogs.

PURPOSE: This study was designed to investigate the effects and mechanisms of anal electric stimulation with long pulses on anal sphincter pressure in conscious dogs. METHODS: The study was performed after enema in nine healthy female hound dogs and composed of four randomized sessions ("dose"-response, anal electric stimulation only, or with atropine or phentolamine). The anal sphincter pressure was measured by using manometry and quantified by using the area under the contractile curve (mmHg/sec). Anal electric stimulation was performed via a pair of ring electrodes attached to a manometric catheter. The stimulation parameters in all but dose-response sessions included a frequency of 20 ppm, pulse width of 200 ms, and amplitude of 3 mA. RESULTS: The anal sphincter pressure was 55.7 +/- 6 at baseline and increased by 37 percent to 76.4 +/- 6.5 during electric stimulation (P = 0.009). The increase of anal pressure during stimulation was positively correlated with the stimulation energy (r = 0.395; P < 0.01). The excitatory effect of electric stimulation was sustained for at least 20 minutes. Atropine did not alter anal pressure and did not abolish the excitatory effect of anal electric stimulation on the sphincter. Phentolamine reduced anal pressure from the baseline value of 50.5 +/- 4.7 to 33.1 +/- 5.4 (P = 0.019). The electric stimulation induced increase in anal pressure was dropped from 19 +/- 2.6 to 9.9 +/- 2.8 (P = 0.029) at the presence of phentolamine. CONCLUSIONS: Anal electric stimulation with long pulses increases anal sphincter pressure in an energy-dependent manner. The alpha-adrenergic but not the cholinergic pathway at least partially mediates the excitatory effect of anal electric stimulation.

Adrenergic alpha-Antagonists↗
PubMed1995

Modulation of noradrenaline release through presynaptic alpha 2-adrenoceptors in congestive heart failure.

Stimulation of presynaptic alpha 2-adrenoceptors inhibits the release of noradrenaline from sympathetic nerve endings; however, the extent to which it operates in patients with congestive heart failure is still unknown. To investigate the degree of negative feedback to the release of noradrenaline via presynaptic alpha 2-adrenoceptors at sympathetic nerve endings, we measured plasma noradrenaline levels before and after the injection of phentolamine (i.e., plasma noradrenaline concentration at rest, plasma noradrenaline concentration after phentolamine injection [NAph], and the phentolamine-induced increase in plasma noradrenaline [delta NAph]). Plasma noradrenaline concentration at rest, NAph, and delta NAph increased in a stepwise manner from New York Heart Association class I to class III. A positive correlation was found between the plasma noradrenaline at rest and delta Naph (n = 123, r = 0.697, p < 0.001). These results suggest that the enhanced release of plasma noradrenaline is substantially buffered by the mechanism of noradrenaline release-inhibitory presynaptic alpha 2-adrenoceptors in patients with congestive heart failure, and this buffer serves to protect organs such as the heart from excess sympathetic stimulation.

Aged↗
PubMed1975

Relation of renin status to neurogenic vascular resistance in borderline hypertension.

The relation of renin-angiotensin status to general hemodynamics and to neurogenic vascular resistance was studied in patients with border-line hypertension. Plasma renin activity during standing was referred to a standard renin-urinary sodium nomogram derived from 18 normal subjects. Among 22 patients with borderline hypertension the renin level was high in 8, low in 4 and within normal limits in the remaining 10. In patients with borderline hypertension and high or normal levels of plasma renin activity, the blood pressure elevation was due to increased total peripheral vascular resistance. In contrast, in patients with low renin borderline hypertension, total peripheral resistance was not significantly elevated; the blood pressure elevation reflected a cardiac index 12 percent higher than that in normal subjects. The neurogenic contribution to total peripheral vascular resistance was assessed by studying the effects of alpha adrenergic blockade with phentolamine, after prior autonomic blockade of the heart with atropine (0.04 mg/kg body weight) and propranolol (0.2 mg/kg). Phentolamine (15 mg) produced an immediate reduction in total peripheral resistance of 12.0 +/- 6.7 percent in patients with high renin borderline hypertension (P less than 0.01) but no change in normal subjects or those with borderline hypertension and normal or low renin levels. Normalization of the blood pressure followed "total" autonomic blockade with atropine, propranolol or phentolamine only in patients with high renin borderline hypertension. It is concluded from these preliminary data that in high renin borderline hypertension the blood pressure elevation is sustained by neurogenic mechanisms. The elevated renin level in these patients is probably an expression of increased sympathetic nervous activity. Although the elevated plasma renin level may possibly be contributing to the generation of higher sympathetic tone, or data do not support a direct role of circulating angiotensin in the maintenance of the elevated vascular resistance.

Adolescent↗
PubMed1980

Umbilical venous blood flow and its distribution before and during autonomic blockade in fetal lambs.

In nine chronically catheterized fetal lambs (120 to 135 days; term 147 days) umbilical venous blood flow and its distribution were measured by the radionuclide-labeled microsphere technique before and during autonomic blockade with atropine (0.20 to 0.25 mg/kg; seven studies) or phentolamine (0.10 to 0.12 mg/kg; six studies). Atropine significnatly increased mean fetal heart rate (182 to 207 beats/min), descending aortic blood pressure (49 to 55 mm Hg), and umbilical venous blood flow (210 to 239 ml/min/kg fetus), without changing umbilical venous blood pressure. Phentolamine decreased mean descending aortic pressure (48 to 45 mm Hg), but did not affect heart rate, umbilical venous blood pressure, or umbilical venous blood flow. Neither atropine nor phentolamine altered the distribution of umbilical venous blood flow to the ductus venosus, the liver, or the other fetal organs. These data indicate that the cholinergic nervous system only indirectly affects the basal umbilical venous blood flow in the near-term fetal lamb. This effect is small and is secondary to associated changes in heart rate and arterial blood pressure. Neither the cholinergic nor the alpha-adrenergic systems influence the basal distribution of umbilical venous blood flow.

Animals↗
PubMed1986

Unsuitability of the 86Rb+ uptake method for estimation of (Na+ + K+)-ATPase activity in innervated tissues.

(Na+ + K+)-ATPase activity was estimated by 86Rb+ uptake in dog saphenous vein to determine the validity of the technique in tissues that have a sympathetic innervation. When saphenous vein rings were incubated at 37 degrees C in Krebs' solution containing 86Rb+, the cardenolide acetylstrophanthidin caused a concentration-dependent inhibition of Rb+ uptake. The threshold for inhibition was approx. 10 nM acetylstrophanthidin and the maximum effect was obtained at 9 microM. In the upper part of this concentration range (greater than 1 microM) acetylstrophanthidin released noradrenaline from the sympathetic nerve terminals associated with the tissue. In this upper part of the acetylstrophanthidin concentration range the alpha-adrenoceptor antagonist phentolamine (8 microM) reduced, by up to 25%, the degree of 86Rb+ uptake inhibition caused by the cardenolide. In other experiments, saphenous vein strips were loaded with 86Rb+ and perifused with Krebs' solution containing acetylstrophanthidin. At concentrations which release noradrenaline, acetylstrophanthidin increased the efflux of 86Rb+. Phentolamine (8 microM) prevented the acetylstrophanthidin-evoked efflux of the isotope as did prior in vitro denervation of 86Rb+ loaded strips with 6-hydroxydopamine. Exogenous noradrenaline (1-100 microM) added to the perifusing fluid also caused an efflux of 86Rb+ that was attenuated by phentolamine. The data indicate for dog saphenous vein that with low concentrations of acetylstrophanthidin the extent of 86Rb+ accumulation might accurately reflect prevailing (Na+ + K+)-ATPase activity. At higher concentrations of acetylstrophanthidin, however, noradrenaline is released from the nerve endings and causes 86Rb+ efflux from the smooth muscle cells consequent upon alpha-adrenoceptor activation. Since this efflux reduces the extent of Rb+ accumulation, measurement of the latter does not adequately reflect uptake mediated by the activity of (Na+ + K+)-ATPase. This is significant because in most applications of the 86Rb+ uptake method it is the estimate of Rb+ accumulation made in the presence of a high concentration of cardenolide that forms the basis of all subsequent calculations with respect to (Na+ + K+)-ATPase activity.

Animals↗
PubMed1982

Uptake and displacement of [3H]dihydroalprenolol, [3H]epinephrine and [3H]clonidine in isolated perfused rabbit lung.

Uptake and displacement of three adrenergic receptor ligands, [3H]dihydroalprenolol ([3H]DHA), [3H]epinephrine ([3H]EPI) and [3H]clonidine ([3H]CLON), were examined in isolated rabbit lungs by recirculating perfusion. Removal of [3H]DHA was the most extensive (85% uptake; 6.6 ml/min clearance), [3H]CLON removal was intermediate (50%; 3.8 ml/min), and [3H]EPI removal was the lowest (33%; 1.2 ml/min). Specific displacement of each radioligand from lung was attempted using several competing agents. Both (--)- and (+)-propranolol equally displaced [3H]DHA from lung. Phentolamine, (--)-phenylephrine and (--)-epinephrine were unable to displace 10 nM [3H]EPI from lung, although the latter two agents did produce concentration-dependent increases in perfusion pressure. High concentrations of (--)-epinephrine, which produced near maximal physiological responses, inconsistently displaced 30-4- nM [3H]EPI from lung. [3H]Clonidine was displaced by unlabeled clonidine at concentrations that caused increases in perfusion pressure. Pretreatment of lungs with either 10 microM phentolamine or phenoxybenzamine did not alter the total amount of [3H]CLON displaced by clonidine, suggesting that [3H]CLON was displaced predominantly from non-specific sites, perhaps preventing detection of [3H]CLON displacement from specific (receptor) sites. Alternatively, these results may be interpreted as inhibition of uptake of each radioligand. Thus, both (--)- and (+)-propranolol interfered with [3H]DHA removal, suggesting a common mechanism for uptake and/or retention for these two beta-adrenergic receptor antagonists. Inhibition of [3H]EPI removal was observed only at high concentrations of (--)-epinephrine which indicates that pulmonary removal of epinephrine occurs through a low affinity uptake system. [3H]Clonidine removal was effectively inhibited by the same (microM) concentrations of unlabeled clonidine that produced physiological responses. Neither phentolamine nor phenoxybenzamine was able to interfere with pulmonary removal of [3H]CLON. Therefore, uptake and displacement of these adrenergic receptor radioligands showed no correlation with pharmacological effects produced by these agents in isolated perfused rabbit lung. The results are more closely associated with inhibition of removal and/or non-specific retention of the radioligands examined.

Alprenolol↗
PubMed1990

Dimethylphenylpiperazinium (DMPP)-induced relaxation and elevation of cyclic GMP content in canine lower esophageal sphincter (LES).

Cyclic GMP has been proposed as an intracellular mediator of neuronally-induced relaxation in lower esophageal sphincter (LES) smooth muscle. If cyclic GMP is indeed an intracellular messenger, then agents that activate enteric neurons of the sphincter [e.g. the ganglionic nicotinic receptor agonist dimethylphenylpiperazinium (DMPP)] also should cause a relaxation that is associated with an increase in cyclic GMP content. In isolated smooth muscle strips of canine LES, DMPP produced a rapid relaxation that was accompanied by a significant (P less than 0.05) increase in cyclic GMP content with no change in cyclic AMP content. Pretreatment of tissues with either tetrodotoxin or hexamethonium antagonized both the DMPP-induced relaxation and the associated increase in cyclic GMP. The combination of phentolamine and meclofenamic acid also antagonized both the relaxation and the elevation of cyclic GMP produced by DMPP. Electrical field stimulation (EFS)-induced relaxation and elevation in cyclic GMP was unaltered by meclofenamic acid and phentolamine. In conclusion, DMPP (like neuronal electrical activation) relaxed isolated canine LES through an enteric neuronal inhibitory pathway. The presence of phentolamine and meclofenamic acid did not affect EFS-induced effects, but blocked both the relaxation and the increase in cyclic GMP produced by DMPP, suggesting a more complicated pathway for DMPP in the release of inhibitory transmitter.

Animals↗
PubMed1981

Noradrenergic responses in rat hippocampus: evidence for medication by alpha and beta receptors in the in vitro slice.

The effect of perfused norepinephrine (NE) on evoked potentials in CA1 of the in vitro rat hippocampus was examined. Weak and variable effects on population spike amplitude were observed, with lower doses of NE generally producing excitations and higher doses more often producing inhibitions. Clonidine, an alpha-receptor agonist, produced a dose-dependent inhibition of population spike amplitude; this inhibition was effectively antagonized by the alpha-antagonist, phentolamine. Isoproterenol (ISO), a beta-agonist, produced marked increases in population spike amplitude which could be antagonized by timolol, a beta-receptor antagonist. Phentolamine did not antagonize the excitations produced by ISO, and timolol had no effect on the inhibitions seen with clonidine. After pretreatment with either phentolamine or timolol, NE perfusion elicited robust and consistent elevations or reductions in the population spike, respectively. A potent cyclic AMP derivative, 8-p-chlorophenylthio cyclic AMP, produced large increases in population spike amplitude which appeared similar to the responses seen with beta-agonists. No changes in field EPSP amplitudes were observed with any of the drugs tested. Taken together, these results suggest that NE may interact with alpha-adrenergic receptors to decrease pyramidal cell excitability, and the beta-adrenergic receptors to increase pyramidal cell excitability; the beta-effect may involve cAMP.

Animals↗
PubMed1981

Hypoalgesia induced by blockade of noradrenergic projections to the raphe magnus: reversal by blockade of noradrenergic projections to the spinal cord.

Previous studies have demonstrated that microinjection of noradrenergic (NA) antagonists such as phentolamine in the nucleus raphe magnus (NRM) produces hypoalgesia. This hypoalgesia appears to result from disinhibition of raphe-spinal serotonergic neurons since it is blocked by intrathecally injected methysergide. The present studies demonstrate that the hypoalgesia produced by microinjection of phentolamine in the NRM is also abolished by intrathecal administration of phentolamine. The results suggest that the hypoalgesia produced by microinjection of NA antagonists in the NRM is also mediated, at least in part, by the activation of spinally projecting NA neurons. Such hypoalgesia does not appear to be mediated by activation of enkephalinergic neurons since intrathecal injection of the opiate antagonist naloxone did not attenuate the hypoalgesia.

Animals↗
PubMed1990

Galanin-induced prolactin release in rats: pharmacological evidence for the involvement of alpha-adrenergic and opioidergic mechanisms.

The mechanism by which galanin (GAL) stimulates prolactin (PRL) secretion was investigated in urethane-anesthetized male rats. The PRL release induced by intracerebroventricular (i.c.v.) injection of porcine GAL (pGAL) was similar to that induced by rat GAL. The PRL release induced by pGAL was partially blocked by alpha-adrenergic antagonists, phentolamine (1 microgram/rat, i.c.v.; 29.1 +/- 4.5 ng/ml vs control 66.9 +/- 10.2 ng/ml, P less than 0.01) and tolazoline (1 microgram/rat, i.c.v.; 25.9 +/- 4.4 ng/ml vs control 59.6 +/- 10.9 ng/ml, P less than 0.05). Neither propranolol (1 microgram/rat, i.c.v.), a beta-adrenergic antagonist, nor prazosin (1 microgram/rat, i.c.v.), an alpha 1-adrenergic antagonist, inhibited pGAL-induced PRL release. Naloxone (125 micrograms/100 g body wt., i.v. 30 min before), an opiate antagonist, also inhibited pGAL-induced PRL release (25.9 +/- 4.0 ng/ml vs 59.1 +/- 7.2 ng/ml, P less than 0.01). Combined treatment with naloxone and phentolamine caused greater inhibition of pGAL-induced PRL release than did phentolamine alone (10.3 +/- 1.5 ng/ml vs 23.2 +/- 4.7 ng/ml, P less than 0.05), but the inhibition was similar to that induced by naloxone alone. These findings suggest that alpha 2-adrenergic and opioidergic mechanisms are involved in PRL release induced by GAL.

Adrenergic alpha-Antagonists↗
PubMed1990

Antagonism of stimulation-produced antinociception from ventrolateral pontine sites by intrathecal administration of alpha-adrenergic antagonists and naloxone.

Focal electrical stimulation of the ventrolateral pontine tegmentum in conscious rats induced antinociception in approximately one-half of the animals screened, as indicated by a marked suppression of the thermally evoked tail-flick flexion reflex. The effectiveness of ventrolateral pontine stimulation in elevating tail-flick latency was significantly reduced by intrathecal microinjection of 30 micrograms of the non-selective alpha-adrenergic antagonist phentolamine, and was largely abolished by a 60-micrograms dose of this drug. The blockade of ventrolateral pontine stimulation-produced antinociception by phentolamine was maximal by 15 min postinjection, and was still evident 60 min after drug microinjection. Ventrolateral pontine stimulation-produced antinociception was also attenuated by intrathecal administration of the alpha 2-selective antagonist yohimbine (37 micrograms) and the opioid antagonist naloxone (30 micrograms), but not the alpha 1 antagonist WB-4101 (37 micrograms), the beta-adrenergic antagonist propranolol (111.6 micrograms) nor the serotonergic antagonist methysergide (30 micrograms). However, the antagonism of pontine stimulation-produced antinociception by naloxone was unlike that of phentolamine and yohimbine, in that it developed slowly and was only evident at 60 min postinjection. Hence naloxone's site of action may be distant from the injection site. These data indicate that the thermal antinociception produced by stimulation of the ventrolateral pons is mediated through spinal alpha 2-receptors and opioid receptors of uncertain location. The close proximity of many of the effective electrode placements to the rostral A5 and ventral subcoerulear A7 noradrenergic cell groups suggests that noradrenergic spinopetal projections arising from these groups are involved in mediating the antinociception induced by stimulating these sites.

Adrenergic alpha-Antagonists↗
PubMed1978

Prazosin and presynaptic alpha-receptors in the cardioaccelerator nerve of the dog.

In vagotomized, spinal-sectioned dogs, prazosin and phentolamine enhanced positive chronotropic responses to cardiac accelerator nerve stimulation. In additional dogs the inhibition by clonidine of heart rate response to continuous accelerator nerve stimulation (presynaptic effect), and the vasopressor effect of clonidine (post-synaptic effect), were antagonized by prazosin, phentolamine and yohimbine; cumulative doses for 50% antagonism of the cardiac chronotropic effect were 103, 50 and 13 microgram/kg i.v., respectively, and those for 50% antagonism of the vasopressor effect were 39, 38 and 3 microgram/kg i.v., respectively. On isolated rabbit pulmonary artery, prazosin antagonized electrically evoked contractions but had no effect on 3H output, whereas yohimbine enhanced both. The results indicate that prazosin, like phentolamine and yohimbine, blocks presynaptic alpha-adrenergic receptors on the cardiac accelerator nerve of the dog but, unlike yohimbine, prazosin does not block these receptors on noradrenergic nerves of rabbit pulmonary artery. It is concluded that the relative activity of a compound at pre- and postsynaptic alpha-receptors is not the same for all organs. The results are discussed relative to the fact that prazosin causes hypotension without significant reflex tachycardia in dog and man.

Animals↗
PubMed1984

Responses of isolated canine intermediate auricular arteries to 5-hydroxytryptamine and methysergide.

The responses of the isolated canine intermediate auricular arteries to 5-hydroxytryptamine (5-HT), methysergide, norepinephrine (NE) and potassium chloride (KCl) were examined by means of the 'cannula inserting' method. 5-HT produced dose-dependent vasoconstriction more potently than did NE. The effect was blocked by methysergide, i.e. a small dose of methysergide competitively inhibited the 5-HT-induced effect, and a large amount of methysergide inhibited it non-competitively. The 5-HT-induced constriction was slightly but significantly suppressed by phentolamine in doses which markedly blocked NE-induced effects. KCl-induced effects were not significantly affected by methysergide and phentolamine treatment. Methysergide induced vasoconstriction by itself in about half out of all preparations. In cases in which methysergide induced vasoconstriction, the dose-response curves were bell-shaped and the constriction became smaller with large doses. At small doses, methysergide induced reproducible vasoconstriction but at large doses it readily caused tachyphylaxis. The methysergide-induced constriction was not blocked by 1 microgram of phentolamine which inhibited NE-induced constriction. It is concluded that the canine intermediate auricular artery is very sensitive to 5-HT and methysergide, and that the action of 5-HT may partially involve alpha-adrenergic mechanisms.

Animals↗
PubMed1984

Insulin suppressive effects of aminotetralin analogs and of dopamine.

The study concerned the effects of 2-amino-6,7-(OH)2-1,2,3, 4-tetrahydronaphthalene (A-6,7-DTN), dipropyl-A-6,7-DTN and dopamine on plasma levels of immunoreactive insulin (IRI) in cattle. During infusions of A-6,7-DTN, dipropyl-A-6,7-DTN and dopamine, the circulating levels of IRI decreased. In response to A-6,7-DTN, the levels of glucose increased whereas non-esterified fatty acids did not change. The decrease of IRI during additional infusions of A-6,7-DTN was not modified by prolonged administration of A-6,7-DTN. During infusions of A-6,7-DTN there was no increase in response to the administration of glucose and tolbutamide. However, if the beta-adrenergic agonist isoproterenol was infused, IRI increased in the presence of A-6,7-DTN. During, infusions of the alpha-adrenergic blocking agent, phentolamine, levels of IRI increased within minutes while glucose did not change. Concomitant infusions of A-6,7-DTN and phentolamine caused IRI to decrease and the rise in glucose levels seen in the absence of phentolamine was inhibited. In conclusion, enhanced dopaminergic activity inhibited IRI secretion. The suppressive effects of A-6,7-DTN were due primarily to its dopaminergic properties, but A-6,7-DTN also possessed some characteristics of an alpha-adrenergic agonist. beta-Adrenergic stimulation reversed the suppressive effects of A-6,7-DTN on IRI secretion.

Animals↗
PubMed1985

The importance of the alpha-adrenoceptor agonist activity of dobutamine to inotropic selectivity in the anaesthetized cat.

Doses of dobutamine (steady-state infusions) required to increase inotropy (as measured by isovolumic indices of contractility) were lower than those required to produce tachycardia in the anaesthetized cat. When compared to isoprenaline, dobutamine produced less tachycardia for common increases in inotropy and thus demonstrated inotropic selectivity in this model. Dobutamine also produced mild pressor effects which were potentiated by beta-adrenoceptor blockade with propranolol. In efforts to define the role of the partial agonist activity of dobutamine for alpha-adrenoceptors in the production of selective inotropy the effects of dobutamine infusions were observed in cats pretreated with the alpha-adrenoceptor antagonist phentolamine. In phentolamine-treated cats dobutamine did not demonstrate inotropic selectivity and showed a relationship between increased inotropy and tachycardia which was not significantly different from that obtained with isoprenaline. In contrast, phentolamine did not change the relationship between isoprenaline-induced tachycardia and increased inotropy. These data suggest that the agonist activity of dobutamine for alpha-adrenoceptors could be responsible for selective inotropy in the anaesthetized cat probably by baroreceptor-mediated reflex modulation of heart rate and/or possible stimulation of inotropic cardiac alpha-adrenoceptors.

Animals↗
PubMed1995

Effects of two endogenous Na+,K(+)-ATPase inhibitors, marinobufagenin and ouabain, on isolated rat aorta.

Previously, we reported that the venom of Bufo marinus toad contains a Na+,K(+)-ATPase inhibitor with potent vasoconstrictor activity. In the present study, using thin-layer chromatography in Silicagel 60 F254 + 366, we separated a vasoactive substance from a mixture of steroids from Bufo marinus venom. Based on chromatographic mobility of this substance and typical color reaction after its vizualization with SbCl3, we identified it as a previously described steroid, marinobufagenin. Vasoconstrictor and Na+,K+ pump inhibitory properties of marinobufagenin were studied in isolated rat aortic rings and compared with those of ouabain. Ouabain (10-100 mumol.1-1) produced weak vasoconstriction, which was blocked by 2 mumol.1-1 phentolamine. 10 mumol.1-1 ouabain stimulated, and at higher concentrations inhibited, the Na+,K+ pump. 2 mumol.1-1 phentolamine abolished the activating effect of 10 mumol.1-1 ouabain on the Na+,K+ pump, but did not alter the inhibitory action of higher concentrations of ouabain. By contrast, marunibufagenin elicited rapid and strong vasoconstriction and inhibited ouabain-sensitive 86Rb uptake. Antidigoxin antibody antagonized the vasoconstrictor responses to marinobufagenin, but not to ouabain. 2 mumol.1-1 phentolamine did not alter the constrictor effect of marinobufagenin. In solid-phase digoxin immunoassay, marinobufagenin demonstrated higher digoxin-like immunoreactivity than ouabain.

Amphibian Venoms↗
PubMed1984

Angiotensin and norepinephrine effects on isolated vascular strips from a reptile.

In order to better understand the vascular effects of angiotensin II (AII) in lower vertebrates, the contractile responses of aortic strips from the freshwater turtle Pseudemys scripta elegans were studied. Circumferential strips from the left aortic arch were suspended in a tissue bath in 25 degrees C reptilian Ringer's solution at pH 7.5. Both [Asn1,Val5] AII (10(-9)-10(-5) M) and norepinephrine (NE) (10(-8)-10(-4) M) produced dose-dependent contractions. The threshold dosage for AII was between 10(-9) and 10(-8) M and for NE between 10(-8) and 10(-7) M. Pretreatment with [Sar1,Ile8] AII (10(-6) M) significantly attenuated the response to [Asn1,Val5] AII at 10(-5) M and totally blocked the response at lower AII concentration (P less than 0.01 in each case). The response to AII was unaffected by phentolamine (10(-6) M). Phentolamine abolished the response to NE at concentrations of 10(-6) M or less (P less than 0.01) and attenuated the response by 48% at 10(-5) M (P less than 0.05) and 43% at 10(-4) M (P less than 0.05) NE. The response to NE was unaffected by [Sar1,Ile8] AII. The results demonstrate that [Asn1,Val5] AII has a direct contractile effect on turtle vasculature and that two functionally distinct vascular receptor populations for AII and NE are present in the turtle. Since phentolamine did not affect the responses to AII, it also appears that angiotensin-evoked norepinephrine release from the sympathetic nerve terminals in the vessel is not involved in the angiotensin-induced contractions in this preparation.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1986

Blood pressure homeostasis in the snake, Ptyas korros.

Three putative pressor systems, the alpha-adrenergic system (AS), the renin angiotensin system (RAS), and the arginine vasotocin system (AVT-S), were studied for their roles in blood pressure regulation and their possible interactions in the rat snake. Ptyas korros. Norepinephrine (NE), angiotensin I (ANG I), and arginine vasotocin (AVT) increased the mean arterial pressure (MAP) of the snake while administration of phentolamine, an alpha-adrenergic antagonist, and captopril, an ANG-converting enzyme inhibitor, but not KBIV24, an AVT antagonist, decreased the MAP. Treatment with any combination of two of these antagonists/inhibitor invariably decreased the MAP. Treatment with the agonist of the remaining third system invariably returned the MAP to normal or above. Phentolamine and KBIV24 attenuated the vasopressor effect of ANG I. Phentolamine and captopril enhanced the vasopressor effect of AVT. The pressor effect of NE was not altered by KBIV24 and captopril. It was concluded that there were at least two pressor systems (AS and RAS) regulating the basal MAP in the snake. There was also interaction among the three systems which could affect the MAP.

Angiotensin I↗