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PubMed1980

Enhanced vascular reactivity to various vasoconstrictor agents following pinealectomy in the rat: role of melatonin.

The mesenteric vascular bed preparation of control and pinealectomized (PX) male Wistar rats was used to examine vascular reactivity to two concentrations each of norepinephrine, serotonin, angiotensin, and potassium. Vasoconstrictor responses to 50- and 100-ng injections of norepinephrine and 0.5- and 1.0-microgram injections of serotonin were 30-40% higher in preparations from PX rats. Reponses to 100 ng but not to 50 ng of angiotensin were also significantly higher in preparations from PX rats. Responses to 1.5- and to 3.0-mg injections of potassium did not differ significantly in either case. In vivo injection of 20 microgram of melatonin 3 h prior to dissection of the preparation, or in vivo perfusion of 20 ng melatonin per millilitre of buffer completely reversed the increased vascular response to all vasoconstrictor agents tested in the PX preparations, but had little effect in control preparations. Also observed in PX rats was a significant increase in blood pressure, serum sodium, and increased body and heart weight. Arterial wall sodium was also elevated in PX rats. These changes may be relevant to the increased vascular reactivity of PX rats. The increased vascular responsiveness of PX rats may be specific for agents that stimulate calcium release from intracellular stores (norepinephrine, angiotensin) rather than those that stimulate calcium influx from extracellular fluid (potassium). Melatonin lack may be the cause of the vascular changes in the PX rats as both in vivo and in vitro it lowered the vasoconstrictor effects of the agents tested, but only in PX rats; it had no significant effect in the control rats.

Angiotensin II↗

PubMed1990

Regional autoregulatory responses during infusion of vasoconstrictor agents in conscious dogs.

We investigated pressure-dependent autoregulatory responses in mesenteric, iliac, and renal vascular beds of conscious dogs during intravenous infusion of angiotensin II, phenylephrine, or arginine vasopressin at rates which increased arterial pressure by 20-40 mmHg. The arteries supplying these beds were instrumented with an electromagnetic flow probe, a nonoccluding catheter, and an electromagnetic flow probe, a nonoccluding catheter, and an occluder cuff connected with a servo-amplifier, which enabled us to return perfusion pressure to control levels during infusion of the vasoconstrictor agents. We attempted to differentiate between the increase in vascular resistance due to the direct effect of the vasoconstrictor agent and the increase induced by an autoregulatory response induced by elevations of aortic perfusion pressure. We measured a strong degree of autoregulation in the renal vascular bed with a fractional compensation value close to 1. Moderate autoregulation occurred in the mesenteric vascular bed, where the compensation was 0.4-0.5 with angiotensin II and phenylephrine and between 0.74 and 0.94 with vasopressin. No autoregulatory capacity could be demonstrated in the hindlimb. The findings indicate that, under conditions of increased systemic blood pressure, both the renal and the mesenteric vascular beds contribute to the increase in total peripheral resistance by pressure-dependent vasoconstrictor responses.

Angiotensin II↗

PubMed1999

Unaltered vasoconstrictor responsiveness after iNOS inhibition in lungs from chronically hypoxic rats.

Previous studies suggest that inducible (i) nitric oxide synthase (NOS) expression within the pulmonary vasculature is increased in rats with chronic hypoxia (CH)-induced pulmonary hypertension. We therefore hypothesized that enhanced iNOS expression associated with CH causes attenuated pulmonary vasoconstrictor responsiveness. To test this hypothesis, we examined the effect of selective iNOS blockade with L-N6-(1-iminoethyl)lysine dihydrochloride (L-NIL) and nonselective NOS inhibition with Nomega-nitro-L-arginine (L-NNA) on vasoconstrictor responses to U-46619 in isolated saline-perfused lungs from both control and CH (4 wk at 380 mmHg) rats. We additionally measured pulmonary hemodynamic responses to L-NIL in conscious CH rats (fraction of inspired O2 = 0.12). Finally, iNOS mRNA levels were assessed in lungs from each group of rats using ribonuclease protection assays. Despite a significant increase in iNOS mRNA expression after exposure to CH, responses to U-46619 were unaltered by L-NIL but augmented by L-NNA in lungs from both control and CH rats. Pulmonary hemodynamics were similarly unaltered by L-NIL in conscious CH rats. We conclude that iNOS does not modulate pulmonary vasoconstrictor responsiveness after long-term hypoxic exposure.

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

PubMed2004

Effect of age on cutaneous vasoconstrictor responses to norepinephrine in humans.

To test the hypothesis that cutaneous vasoconstrictor responsiveness to exogenous norepinephrine is reduced in older compared with young subjects, dose-response relations between norepinephrine and skin blood flow were established. Seven doses of norepinephrine (1.10(-8) to 10(-2) log M) were perfused (2 microl/min) intradermally (4 min/dose) using cutaneous microdialysis (2 probes/subject). To account for possible differences in endogenous norepinephrine between groups, one microdialysis probe was perfused with bretylium tosylate to locally block noradrenergic vesicle release before establishing the norepinephrine dose-response relations. Skin blood flow was indexed via laser-Doppler flowmetry directly over both microdialysis probe sites and is expressed as cutaneous vascular conductance (laser-Doppler flux/mean arterial blood pressure). Local skin temperature was maintained at 34 degrees C at both sites throughout the protocol. Dose-response relation between norepinephrine and cutaneous vascular conductance was similar between control and bretylium-pretreated sites in young subjects (EC50 = -5.18 +/- 0.27 and -5.03 +/- 0.27 log M, respectively). In contrast, the dose-response relation was significantly shifted to the right (i.e., a higher dose of norepinephrine was needed to produce the same vasoconstrictor response) in the bretylium-pretreated site in older subjects (EC50 = -5.46 +/- 0.23 and -4.53 +/- 0.23 log M, respectively). Significant increases in EC50 were observed in older compared with young subjects at the bretylium-pretreated but not the control sites. These data indicate that cutaneous vasoconstrictor responsiveness is decreased in older subjects when endogenous release of norepinephrine is antagonized. Furthermore, these findings suggest that differences in presynaptic norepinephrine release between older and younger subjects are profound enough to affect dose-response relations between norepinephrine and cutaneous vascular conductance.

Adolescent↗

PubMed1999

Analysis of vasoconstrictor responses to histamine in the hindlimb vascular bed of the rabbit.

Hemodynamic responses to histamine were investigated in the anesthetized rabbit. Intravenous injections of histamine induced dose-dependent decreases in systemic arterial pressure that were blocked by the H(1)-receptor antagonist pyrilamine but not the H(2) antagonist cimetidine. Injections of histamine and the H(1) agonist 6-[2-(4-imidazolyl)ethylamine]-N-(4-trifuormethylphenyl)-heptan ecardo xamide dimaleate (HTMT) into the hindlimb perfusion circuit increased hindlimb perfusion pressure, whereas the H(2) agonist dimaprit decreased perfusion pressure and the H(3)-receptor agonist R-(-)-alpha-methylhistamine did not alter perfusion pressure. Pyrilamine reduced hindlimb vasoconstrictor responses to histamine and HTMT but did not alter vasodilator responses to dimaprit. Cimetidine reduced the response to dimaprit but did not alter vasoconstrictor responses to histamine or HTMT. The H(3)-receptor antagonist thioperamide was without effect on responses to the histamine agonists. These data suggest the presence of H(1) and H(2) receptors and that histamine for the most part acts by stimulating H(1) receptors to produce vasoconstriction in the hindlimb vascular bed of the rabbit. Responses to histamine, HTMT, and norepinephrine were significantly enhanced by a nitric oxide synthase inhibitor at a time when vasodilator responses to dimaprit were unaltered and responses to acetylcholine were significantly reduced. Responses to histamine and the H(1) and H(2) agonists were not affected by the cyclooxygenase inhibitor meclofenamate or by ATP-sensitive K(+) channel, alpha-adrenergic, or angiotensin AT(1) receptor antagonists. The present data suggest that H(1) receptors mediate both systemic vasodepressor and hindlimb vasoconstrictor responses to histamine.

Adamantane↗

PubMed1990

Prostaglandin influences on afferent arteriolar responses to vasoconstrictor agonists.

The present study was designed to evaluate, at the microvascular level, the ability of prostaglandins E2 (PGE2) and I2 (PGI2) to counteract the afferent vasoconstrictor effects of angiotensin II (ANG II) and norepinephrine (NE). The renal microvasculature of rats pretreated with captopril and indomethacin was studied directly by use of the in vitro blood-perfused juxtamedullary nephron technique combined with videomicroscopy. Afferent arterioles averaged 22.7 +/- 0.6 microns ID (n = 59) under control conditions. Topical administration of PGE2 revealed a concentration-dependent afferent vasoconstriction, whereas PGI2 (10(-7) to 10(-5) M) failed to significantly alter afferent arteriolar diameter. Afferent arterioles constricted during exposure to either 10(-9) M ANG II (-15 +/- 3%, n = 13) or 10(-7) M NE (-19 +/- 3%, n = 13). Addition of PGE2 (10(-6) M) to the bathing solution enhanced the vasoconstrictor influences of ANG II and NE by an additional 18 +/- 6 and 13 +/- 4%, respectively. In contrast, while 10(-6) M PGI2 had no effect on ANG II-induced afferent vasoconstriction, it did produce a 30% attenuation of NE-induced constriction. Furthermore, pretreatment of the tissue with 10(-6) M PGI2 prevented development of NE-induced afferent vasoconstriction. Thus, although local tissue prostanoid concentrations are unknown, it appears that low micromolar concentrations of PGE2 elicit an afferent arteriolar constriction that can accentuate the vascular actions of ANG II and NE on rat juxtamedullary afferent arterioles. In contrast, PGI2 can counteract the vasoconstrictor response to NE, but not ANG II, in this experimental setting.

Afferent Pathways↗

PubMed1999

Effects of acute and chronic exercise on vasoconstrictor responsiveness of rat abdominal aorta.

Reductions in blood pressure that are associated with exercise training have been hypothesized to be the result of a sustained postexertional vascular alteration following single bouts of exercise. The purpose of this study was to determine whether a decrease in vascular sensitivity to vasoconstrictor agonists occurs after a single bout of exercise and whether this vascular alteration is sustained through various periods of exercise training. Vascular responses of abdominal aortic rings to norepinephrine (NE; 10(-9)-10(-4) M) were determined in vitro. Aortas were isolated from sedentary rats immediately after rats performed a single bout of treadmill exercise (30 m/min for 1 h); 24 h after the last exercise bout in rats exercised for 1 day; and 1, 2, 4, and 10 wk of training at 30 m/min, 60 min, 5 days/wk. Sensitivity to NE was only diminished after 10 wk of training. This diminished vascular sensitivity to NE was abolished with the removal of the endothelial cell layer. Furthermore, there were no reductions in developed tension or vascular sensitivity to the vasoconstrictor agonists KCl (10-100 mM), phenylephrine (10(-8)-10(-4) M), and arginine vasopressin (10(-9)-10(-5) M) in vessels either with or without the endothelial layer after a single bout of exercise. These data indicate that a single bout of exercise does not diminish aortic responsiveness to vasoconstrictor agonists and thus is not responsible for the diminished contractile responsiveness that occurs between 4 and 10 wk of moderate-intensity exercise training in rats. This vascular adaptation to exercise training appears to be mediated through an endothelium-dependent mechanism.

Adrenergic alpha-Agonists↗

PubMed1994

Vascular reactivity to vasoconstrictors in aorta and renal vasculature of hyperthyroid and hypothyroid rats.

Vascular reactivity to vasoconstrictors in relation to altered thyroid function was studied in two preparations: aortic strips and the isolated perfused kidney. To assess whether the possible alterations in vascular reactivity were restricted to a specific agonist or whether they involved the contractile system, receptor-mediated and nonspecific smooth muscle stimulants were used. Male Wistar rats were divided into three groups: control, hyperthyroid and hypothyroid rats. Aortic strips from hypothyroid rats were less sensitive to phenylephrine and KCl when the data were expressed in absolute values or as percentages of the maximum responses. Sensitivity and reactivity in strips from hyperthyroid rats were similar to those observed in control strips. Renal vasculature obtained from hypothyroid rats also showed a markedly reduced sensitivity to phenylephrine, with normal maximal responses. The response to vasopressin at 3-10(-11) mol/l was also decreased, as was the reactivity to barium chloride. In contrast, renal vasculature of hyperthyroid rats showed markedly enhanced reactivity to all agonists: the concentration-response curves were characterized by a similar threshold and a greater maximal response. These results demonstrate that hypothyroidism is accompanied by a marked decrease in sensitivity to vasoconstrictors in large arteries as well as in resistance vessels. This decrease may be secondary to a generalized alteration in the contractile system of vascular smooth muscle cells and may play a role in the decreased blood pressure in these animals. In contrast, isolated perfused kidneys of hyperthyroid rats showed increased vascular reactivity to vasoconstrictors, which may play a role in the maintenance of elevated blood pressure in these animals.

Animals↗

PubMed2001

Attenuated agonist evoked vasoconstrictor responses in the perfused mesenteric vascular bed of streptozotocin diabetic rats.

We compared agonist-evoked responses in the perfused mesenteric vascular bed (MVB) of streptozotocin (STZ) diabetic Sprague-Dawley rats 2 and 14 weeks after induction of diabetes. Endothelin-1 (ET-1)-, methoxamine (MTX)-, and KCl-evoked vasoconstrictor responses were unchanged in 2-week-old diabetic rats. In contrast, both the sensitivity (P < 0.01) and the maximal vasoconstrictor responses (P < 0.05) to ET-1 were attenuated in 14-week-old diabetic rats, whereas endothelin plasma levels were increased (P < 0.05). Although no differences were observed in responses to KCl in either the 2- or 14-week-old diabetic groups, MTX-evoked maximal responses were attenuated in the 14-week-old group (P < 0.01). Changes in agonist-evoked responses in the 14-week-old diabetic group were unaffected by the protein kinase C (PKC) inhibitor, staurosporine, the phospholipase C (PLC) inhibitor, U73122, the calcium channel blocker, nifedipine, the calcium pump inhibitor, cyclopiazonic acid (CPA), or by endothelial denudation. Sodium fluoride (NaF), an activator of guanosine triphosphate binding proteins (G proteins) normalized the responses in the 14-week-old diabetic group. These data suggest that advanced stages of STZ are associated with alterations in G protein receptor coupling and/or activity leading to the attenuation of responses to vasoconstrictor agonists.

Animals↗

PubMed1992

Comparison of vasoconstrictors for functional endoscopic sinus surgery in children.

Three different vasoconstricting agents were evaluated during functional endoscopic sinus surgery (FESS) in 57 children. Oxymetazoline hydrochloride 0.05%, phenylephrine hydrochloride 0.25%, or cocaine 4% was applied to the nasal mucosa in a prospective, randomized, double-blind fashion. Heart rate and blood pressure changes were recorded 5 and 10 minutes after application of the study vasoconstrictor to each nostril. The surgeon's subjective impressions of bleeding and visualization were recorded for each side of the nose, as were total blood loss and anesthesia time. Although all three vasoconstrictors were tolerated well by the children, there was a suggestion that heart rate decreased more at 5 minutes with phenylephrine than with oxymetazoline or cocaine (P = .08) and that blood pressure increased more at 10 minutes with phenylephrine than with oxymetazoline or cocaine (P = .1). No arrhythmias were noted. Subjective scoring for bleeding showed that children receiving oxymetazoline were less likely to receive scores of "more" bleeding than usual (3/38 vs. 10/34 for phenylephrine and 10/35 for cocaine, P less than .02). Subjective scoring for visualization showed that children receiving oxymetazoline were also less likely to receive scores of "worse" visualization than usual (3/38 vs. 12/38 for phenylephrine and 9/35 for cocaine, P less than .01). There was no difference in surgical bleeding or visualization between children receiving phenylephrine and children receiving cocaine. In our institution, 0.05% oxymetazoline is the preferred vasoconstrictor for FESS in children.

Blood Pressure↗

PubMed1997

The role of basally synthesized nitric oxide in modulating the renal vasoconstrictor action of angiotensin II.

Interactions between nitric oxide (NO) and angiotensin (ANG) II in renal vascular beds were examined in anesthetized dogs. The renal blood flow (RBF) response to an intrarenal arterial injection of ANG II was significantly augmented by intrarenal infusion of the NO synthase inhibitor N(G)-nitro-L-arginine (LNA, 50 microg/kg/min). The simultaneous intrarenal infusion of L-arginine (1 mg/kg/min) prevented the potentiating action of LNA. Similar potentiation was also seen in phenylephrine-induced renal vasoconstriction. Moreover, during simultaneous intrarenal infusion of sodium nitroprusside (SNP), an NO donor, the potentiating action of LNA on the renal vasoconstrictor action of ANG II disappeared. Under these conditions, the released NO stimulated by ANG II was still inhibited by LNA, if present, but basally released NO was resupplied by SNP, as indicated by the return of the RBF. During an infusion of phenylephrine, which produced an increase in renal vascular tone similar to that observed during the infusion of LNA, the renal vasoconstrictor action of ANG II was not augmented. These data suggest that basally released NO plays an important role in the regulation of renal hemodynamics by modulating the renal vasoconstrictor actions of ANG II and phenylephrine.

Angiotensin II↗

PubMed1976

The local anesthetic activity of saxitoxin alone and with vasoconstrictor and local anesthetic agents.

STX (saxitoxin), alone and with various vasoconstrictor and local anesthetic agents, was evaluated for its ability to produce topical anesthesia on the rabbit cornea, peripheral nerve block in the rat, and epidural anesthesia in the dog. High frequency and long duration of block can be attained if sufficiently high concentrations of STX are used, although latency is long and the doses used may produce systemic toxicity. Frequency of satisfactory blocks and mean duration of block can be increased and systemic toxicity reduced if STX is administered with a vasoconstrictor agent. Conventional local anesthetic agents also enhance the nerve blocking activity of STX. When appropriate concentrations of STX, vasoconstrictor and local anesthetic agents are used, systemic toxic effects are not manifested and the blocks produced exhibit the rapid onset and high frequency of block characteristic of the local anesthetic agent and the remarkably long duration of STX.

Anesthesia, Epidural↗

PubMed2001

Signaling mechanisms for the selective vasoconstrictor effect of norbormide on the rat small arteries.

Norbormide (NRB) is a selective vasoconstrictor agent of the rat small vessels. The mechanisms underlying the selective vasoconstrictor effect of NRB are unknown. To investigate whether phospholipase C (PLC) signaling pathway plays a role in NRB-induced vasoconstriction, we performed experiments in NRB-contracted tissues, namely, rat caudal arteries (RCA) and smooth muscle cells derived from rat mesenteric arteries (MVSMCs). An NRB-insensitive vessel, namely rat aorta (RA), served as a control tissue. In RCA and RA we measured either isometric tension or formation of inositol phosphates (IPs), the latter taken as an index of PLC activation. In MVSMCs, we measured intracellular free calcium concentration ([Ca2+]cyt). In the presence of external Ca2+, NRB (2-50 microM) stimulated IPs formation in RCA but not in RA, and increased [Ca2+]cyt in MVSMCs. In the absence of external Ca2+, NRB (50 microM) increased IPs formation in RCA but was unable to increase [Ca2+]cyt in MVSMCs. In RCA, in the presence of external Ca2+, NRB-induced contraction was inhibited by calphostin C (0.2-1 microM), an inhibitor of protein kinase C (PKC), and by SK&F 96365 (30 microM), an inhibitor of the store-operated calcium channels, but was poorly affected by verapamil, an L-type calcium channel blocker. However, verapamil was much more effective when external Ca2+ was substituted by Sr2+. These results suggest that NRB elicits its tissue and species-selective vasoconstrictor effect by stimulating PLC-PKC pathway and increasing Ca2+ influx through both verapamil-sensitive and -insensitive calcium channels. Ca2+ release from sarcoplasmic reticulum seems not involved in NRB vasoconstriction.

Animals↗

PubMed1999

[Alterations of arterial vasoconstrictor responsiveness in rats during and after tail-suspension].

Objective. To characterize the time course of alterations in vasoconstrictor properties of arteries during simulated weightlessness, and to examine whether these alterations are reversible. Method. The tail-suspended rat model was used to simulate weightlessness, and the alterations in vasoconstrictor response were examined in vitro using isolated arterial rings. Result. Compared with that of controls, contractile tension evoked by KCl and phenylephrine (PE) were lower in abdominal aortic, mesenteric and femoral arterial rings from 2 wk tail-suspended rats (P<0.05); after 4 wk tail-suspension, the responses of mesenteric and femoral arterial rings to KCl or PE were further decreased (P<0.05); but contraction responses of arterial rings from 8 wk tail-suspended rats were similar to that of 4 wk simulated microgravity rats. The reversibility of altered arterial vasoreactivity after 4 wk tail-suspension was observed for 5 wk. Vasoreactivity of abdominal aortic rings was recovered after first week of recovery, but it took five weeks that altered vasoreactivity of mesenteric and femoral artery got back to normal. Conclusion. The alterations in constrictor properties of arteries are dependent on both the duration of tail-suspension and the position of artery, the diminished vasoconstrictor properties appear to reach a new steady state after 4 wk tail-suspension, and the changes are reversible.

Animals↗

PubMedDate not supplied

Alterations in monitored vital constants induced by various local anesthetics in combination with different vasoconstrictors in the surgical removal of lower third molars.

The purpose of this study was to observe the hemodynamic changes during surgical extraction of lower third molars induced by three local anesthetics solutions associated with different vasoconstrictors. A double-blind observational and longitudinal study was made of 45 healthy adult volunteers subjected to surgical removal of an impacted lower third molar under local anesthesia. Three groups were established (n = 15) according to the anesthetic solution and associated vasoconstrictor administered (4% articaine + epinephrine 1:200,000; 3% mepivacaine without vasoconstrictor; and 3% prilocaine + felypressin 1:1,850,000). Heart rate, systolic and diastolic pressure, and oxygen saturation were recorded at different times before, during and at the end of surgery, along with the type and amount of anesthetic solution administered. The study variables were found to be more stable with articaine + epinephrine 1:200,000, although the three studied solutions caused no significant hemodynamic changes with respect to the basal values when administered in healthy patients subjected to surgical removal of a lower third molar.

Adolescent↗

PubMed1988

New 1,4-dihydropyridines with vasoconstrictor action through activation of Ca++-channels.

We found four new phenylcarbamoyl-substituted 1,4-dihydropyridines which produced vasoconstrictor and vasopressor effects and we further investigated the mode of vasoconstrictor action of one of the derivatives, 2-(2-pyridil)ethyl-4-(2-chlorophenyl)-2,6-dimethyl-5-phenylcarbamo yl-1, 4-dihydropyridine-3-carboxylate (YC-170). In anesthetized dogs. YC-170 (0.1-3 mg/kg i.v.) produced dose-dependent increases in blood pressure, total peripheral resistance and maximum dLVP/dt with slight reductions of heart rate and aortic blood flow. Intracoronary injection of YC-170 (10-1000 micrograms) produced not only a decrease in coronary blood flow but also an immediate reversal of the coronary vasodilation induced by nicardipine (3 micrograms). YC-170 (0.1-3 mg/kg i.v.) also produced a dose-dependent and reversible vasopressor effect in both anesthetized and pithed rats. The vasopressor response to YC-170 in pithed rats was not attenuated by either hexamethonium, prazosin, yohimbine, ketanserin or reserpine but was antagonized by either nicardipine, nifedipine, verapamil or diltiazem. In isolated rabbit aorta, YC-170 (3 X 10(-6) to 3 X 10(-5) M) induced a dose-dependent and reversible contraction which was not affected by either phentolamine, prazosin, mepyramine, ketanserin or atropine but removed by either nicardipine, verapamil or a Ca++-free medium. YC-170 (1 X 10(-6) to 3 X 10(-5) M) displaced [3H]nitrendipine binding to the canine cardiac membrane in an apparently competitive manner with a Ki value of 1.7 X 10(-6) M. The results suggest that the new phenylcarbamoyl-substituted dihydropyridines, including YC-170, exert a direct vasoconstrictor effect, which appears to be associated with an influx of Ca++ through Ca++ channels.

Animals↗

PubMed1982

Vasoconstrictor response of arterioles of the hamster cheek pouch to norepinephrine, prostaglandin H2, F2 alpha and carbocyclic thromboxane A2, a possible thromboxane A2 analogue.

Activated platelets produce thromboxane A2, a potent vasoconstrictor, which may play an important role in pathophysiological disturbances of microcirculation. Thromboxane A2 has a very short half life and has neither been isolated nor synthesized. Hence, the recently reported stable analogue, carbocyclic thromboxane A2 (CTA2), may become an interesting tool in pharmacological research. Its vasoconstrictor potency was compared in vivo with norepinephrine, prostaglandin H2 and F2 alpha using the following method: vessels of a hamster cheek pouch preparation were exposed to a superfusion to which the respective compounds were added to give 1 ng/ml to 0.1 mg/ml final concentrations. The decrease of vessel diameters was measured microscopically. Prostaglandin H2 was found to be the most potent vasoconstrictor followed by CTA2 and norepinephrine. Prostaglandin F2 alpha was least effective. The respective maximal vasoconstrictory responses did not differ significantly.

Animals↗

PubMed1981

A comparison of the vasoconstrictor effects of angiotensin II and angiotensin III in the canine renal vasculature.

The effects of angiotensin II and angiotensin III on systemic blood pressure and renal blood flow were studied in pentobarbital anesthetized dogs pretreated with phenoxybenzamine. Angiotensin II was more potent than angiotensin III in increasing systemic blood pressure when given intravenously. When angiotensin II and angiotensin III were administered directly into the renal artery, angiotensin II was also more potent than angiotensin III as a renal vasoconstrictor. Indomethacin potentiated the responses to angiotensin II and angiotensin III to the same extent. The results indicate that differential vasoconstrictor effects of the two peptides in renal vasculature contribute to the difference in potency of intravenously administered peptides on systemic blood pressure, and also suggest that vasodilator prostaglandins are involved in the vasoconstrictor properties of the two peptides in the renal vasculature of the dog.

Angiotensin II↗