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At least 19 recordsLinked to original sources
PubMed1976

Inhibition of the adrenalectomy-induced increase in plasma renin concentration by vasoconstrictor agents in rats.

Plasma renin concentrations in rats increase after bilateral adrenalectomy without sodium substitution. The effects of i.v. infused (asp1-beta-amid, val5)-angiotensin II (1 mug/kg min), felypressin (phen2, lys8-vasopressin) (40 mU/kg min) and phenylephrine (30 mug/kg min) were investigated on the increase in plasma renin concentration. These effects of the agents were compared with their actions on blood pressure, heart rate and renal hemodynamics. In rats with destroyed macula densa cells the effect of bilateral adrenalectomy without sodium substitution was also studied. Adrenalectomy still increased the plasma renin concentration. Angiotensin II and felypressin, also depressed under these conditions the elevation of plasma renin concentration caused by adrenalectomy. The mechanism of the adrenalectomy-induced renin release and its suppression by vasoconstrictor agents is discussed.

Adrenalectomy↗
PubMed1979

[The use of vasoconstrictor agents in low concentration as additives to local anesthetics in ambulatory maxillofacial interventions].

The authors studied in several test series the suitability of adrenaline and noradrenaline as vasoconstrictor additives to 2% Xylocitin, in a concentration of 1:100,000. At this concentration, noradrenaline proved well suited in tooth extractions. The vasoconstrictor effect of adrenaline is sufficient in all maxillofacial interventions on an outpatient basis.

Anesthesia, Dental↗
PubMed1978

Prostaglandin D2 (PGD2)--a potent coronary vasoconstrictor agent in the guinea pig isolated heart.

The action of prostaglandin D2 (PGD2) on myocardial force of contraction (MFC) and coronary vascular resistance (CVR) was studied in the isovolumetrically perfused guinea pig heart at constant driving frequency (180 beats/min). PGD2 (2 . 10(-9) - 1 . 10(-6) M) produced a concentration-dependent increase in the CVR while the MFC remained unchanged. The ED50 (50% of maximum response) of the coronary vasomotor action amounted to 4.3 . 10(-8) M PGD2. The results give evidence for a potent coronary vasoconstrictor activity of PGD2.

Animals↗
PubMed1978

[Cardiovascular behavior after local anesthesia in the jaw region with added vasoconstrictor agents].

The authors studied the cardiovascular behaviour after injection of different amounts of xylocitin added with adrenalin (1:80 000) and noradrenalin (1:20 000), respectively. The evaluation of the blood-pressure values, pulse rates and electrocardiograms leads to the conclusion that noradrenalin produces considerable side effects at the above-mentioned concentration. The well-known headache phenomena caused by the addition of noradrenalin are analysed.

Anesthesia, Dental↗
PubMed1979

Evidence for Na-retaining humoral agents and vasoconstrictor humoral agents in hypertension-prone Dahl 'S' rats. Prevention of NaCl-induced hypertension in Dahl 'S' rats with thiazide.

Dahl 'S' rats become hypertensive when fed a high NaCl diet but remain normotensive on a low NaCl diet. Dahl 'R' rats are normotensive on either diet. For a given perfusion pressure, isolated 'S' kidneys excrete 50% less Na than 'R' kidneys. Therefore, we searched for a Na-retaining hormone in 'S' rats. Kidneys were isolated without ischemia from normal rats and were continuously perfused at 125 mm Hg with blood from Dahl 'S' and 'R' rats, all on low NaCl diets. Kidneys and adrenals had been extirpated from the perfusing rats. During 15 min of perfusion, the isolated 'normal' kidneys excreted a mean of 164 micronEq of Na/min/100 g during 26 perfusion experiments with blood from 'R' rats. The 'normal' kidneys excreted a mean of 84 micronEq Na during 24 perfusions with blood from 'S' rats. Thus, the normal kidneys excreted half as much Na when perfused with 'S' blood compared with 'R' blood (p less than 0.02). Seemingly, a Na-retaining humoral agent is present in the blood of 'S' rats on a low Na diet in the absence of renal and adrenal tissue. Moreover, in these normal kidneys, perfusion with 'S' blood induced a 16% higher renal vascular resistance than perfusion with 'R' blood (p less than 0.01), indicating vasoconstricting agents in 'S' blood. However, the Na-retaining humoral effect in 'S' blood could lead to Na retention by 'S' kidneys in vivo, which could partially account for the susceptibility of 'S' rats to NaCl hypertension. Hypertension in Dahl 'S' rats can be almost completely prevented by concomitant treatment with thiazide diuretics which act mainly on the kidney to facilitate Na excretion. This result is in agreement with the hypothesis that a shift in the pressure natriuresis curve, reducing Na excretion for a given arterial pressure, is partially responsible for the great sensitivity to NaCl hypertension in the 'S' rat. The Na-retaining hormone may contribute to this shift.

Animals↗
PubMed1979

Mechanism of hyperosmolarity inhibition of vascular contractility.

Studies were made of the responses of the vascular bed of cat hind leg to intraarterial injection of noradrenaline, angiotensine, tyramine and vasopressine, as well as of carotid occlusion upon increasing the tissue osmolarity through intraarterial hypertonic infusion. The limb was perfused at constant blood flow. Hyperosmolarity inhibited the contractile effects of all stimuli studied. The inhibition of the contractility was greater in the case of tyramine and identical in the case of the remaining vasoconstrictor agents. Increased KCl content or the addition of L-ascorbic acid to the hypertonic solution with preservation of the same hyperosmolarity reduced the inhibition of the contractile responses to noradrenaline and angiotensine. The restoration of the contractility was much more pronounced upon simultaneous increase in the KCl content and addition of L-ascorbic acid. No recovery of the contractile effect of tyramine was observed. The mechanism of hyperosmolarity inhibition of the vascular contraction is discussed. In all vasoconstrictor stimuli the inhibition is connected primarily with disruption of the transmembrane exchange of Na+ and Ka+. In some vasoconstrictor agents, e. g. tyramine, there is disturbance in the specific mechanism connected secondarily with vascular contraction.

Angiotensin II↗
PubMed1978

Drug-induced contractile responses in the isolated posterior communicating cerebral artery of the cat.

The isolated posterior communicating cerebral artery of the cat has been shown to have the ability to produce a contractile response to the following drugs; norepinephrine (NE), tyramine (Ty), 5-hydroxytryptamine (5-HT), histamine (H), acetylcholine (Ach) and potassium (K+). The changes in the contractile response were dose-dependent. The order of potencies of these vasoactive agents with respect to ED50 was: 5-HT greater than NE greater than Ach = H = Ty greater than K+. With regard to their ability to induce maximal contractile responses the order was: H = Ach greater than 5-HT = Ty greater than NE = K+. These results show that cerebral arteries are more sensitive to 5-HT than to NE, as opposed to extracranial arteries in which NE is generally the most potent vasoconstrictor agent.

Animals↗
PubMed1975

The influence of temperature increase, elevation of extracellular h+-concentration, and of triiodothyronine on the actions of phenylephrine, histamine, and beta-sympathomimetic drugs on rabbit aortic strips.

In the isolated preparation from the rabbit thoracic aorta, the affinities of the vasoconstrictor agents phenylephrine and histamine, as well as of the vasodilator beta-sympathomimetic drugs isoprenaline, fenoterol (TH 1165a), terbutaline, and salbutamol under the conditions of temperature increase, triiodothyronine and decrease of extracellular pH were investigated. It was observed that (1) a temperature increase from 25 degrees to 42 degrees C significantly indreased the maximal tension evoked by histamine, whereas that induced by the alpha-sympathomimetic drug phenylephrine was not altered significantly; the maximal relaxation caused by beta-sympathomimetic drugs either at 25 degrees or at 42 degrees C did not differ from one another; (2) the affinities of histamine, phenylephrine and of the beta-sympathomimetic drugs isoprenaline, fenoterol, terbutaline, and salbutamol each were comparable at either 25 degrees or 42 degrees C; the rank order of efficacy of the beta-sympathomimetic drugs is isoprenaline greater than fenoterol greater than salbutamol greater than terbutaline; (3) a decrease of the pH from 7.37 to 7.15 diminished the affinities of histamine and of the beta sympathomimetic drugs whereas that of the alpha-adrenergic drug phenylephrine was not altered. A further decrease of the pH to 6.8 diminished additionally the affinity of histamine and of isoprenaline, and especially that of the other beta-sympathomimetic drugs to such an extent that in the latter case complete dose-response curves could not be determined any more; (4) pretreatment of the animals with 0.4 mg/kg of triiodothyronine (T3) for two days, which strongly depressed the tension induced by either histamine or phenylephrine, did not alter the affinity of both drugs; T3 in vitro (10(-6) M) only diminished the affinity of histamine but left that of phenylephrine unaltered; pretreatment for two days with 0.2 mg/kg of T3 yielded a significant diminution of the pD2-values for two beta-sympathomimetic drugs investigated, namely isoprenaline and fenoterol; also the administration of T3 in vitro in a final concentration of 10(-6) M resulted in a diminution of the affinity of both beta-sympathomimetic drugs; (5) the results obtained show that also on the aorta beta-adrenoceptor stimulants are dependent on the metabolic state while alpha-adrenoceptor stimulants are not.

Adrenergic beta-Agonists↗
PubMed1979

Depressed responsiveness to vasoconstrictor and dilator agents and baroreflex sensitivity in conscious, newborn lambs.

The effects of vasoconstrictors and vasodilators were compared in conscious, newborn lambs and adult sheep instrumented with electromagnetic flow probes on the ascending aorta and catheters in the thoracic aorta. Methoxamine, angiotensin II, norepinephrine, nitroglycerin and isoproterenol were administered intravenously to evaluate their effects on arterial pressure, cardiac output and systemic vascular resistance (SVR). The difference in response between adults and newborns was most apparent with methoxamine. Methoxamine, 400 micrograms/kg, i.v., which increased mean arterial pressure by 57 +/- 6% and SVR by 278 +/- 27% in newborn lambs, caused greater increases (p less than 0.01) of 81 +/- 8% and 1418 +/- 141%, respectively, in the adults. Responses also differed significantly between newborn and adult animals to norepinephrine, angiotensin II, nitroglycerin and isoproterenol. In a second group of animals in which smaller amounts of methoxamine and isoproterenol were injected directly into the terminal aorta, changes in terminal aortic flow and resistance were examined. Again, both vasoconstrictor and vasodilator responses were more marked in adults than in newborns. Finally, the sensitivity of the arterial baroreceptor reflex was evaluated by comparing the regression of pulse interval (PI) on systolic arterial pressure (SAP) after an intravenous dose of methoxamine in conscious, adult and newborn animals. The PI/SAP slopes in adult sheep, 45.4 +/- 3.5 msec/mm Hg, were significantly greater (p less than 0.01) than in newborn lambs, 11.7 +/- 2.2 msec/mm Hg.

Angiotensin II↗
PubMed1976

Prostaglandins and local circulatory control.

The present paper reviews several lines of investigation have provided highly suggestive evidence for an important regulatory role for prostaglandins in the microcirculation. Aside from their profound vasodepressor effects in a number of animal species, including man, and their vasodilator activity in many local circulatory beds, endogenously administered prostaglandins of the E and A type also appear to reduce vascular responsiveness to a variety of vasoconstrictor agents. Furthermore, inhibition of endogenous synthesis and release of prostaglandins leads to a potentiation of vasoconstrictor responses. Thus it appears that the release of prostaglandins, an event that accompanies or is a consequence of vasoconstriction, can moderate the constrictor response and in this manner can contribute to the control of vascular reactivity. Administration of inhibitors of prostaglandin synthesis to tissues that under basal experimental conditions release prostaglandins, causes not only a decrease in prostaglandin output but also an increase in resting perfusion pressure. These results support the concept that prostaglandins that are released are essential in the control of vascular tone and resistance. Other evidence also suggests that prostaglandins participate in a variety of vascular responses, including the mediation of bradykinin vasodilation, functional hyperemia, and reactive hyperemia.

5,8,11,14-Eicosatetraynoic Acid↗
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↗
PubMed1976

The effects of 2-phenylalanine 8-lysine vasopressin (octapressin) on blood vessels in the rat tail.

Isolated perfused segments of the ventral rat tail artery have been used in this study to investigate the effects of octapressin on vascular smooth muscle and its interaction with other vasoconstrictor agents. It was found that repeated octapressin administration was associated with tachyphylaxis and that the onset and rate of development of this phenomenon could be modified by cocaine. The constrictor action of catecholamines, electrical stimulation and serotonin on the rat tail artery was potentiated by octapressin. Mechanisms which may be involved in octapressin tachyphylaxis are discussed.

Angiotensin II↗
PubMed1978

Changes of vascular reactivity induced by low vasopressin concentrations: interactions with cortisol and lithium and possible involvement of prostaglandins.

Arginine vasopressin in physiological concentrations potentiated the vascular effects of various vasoconstrictor agents. By using the isolated rat mesenteric artery preparation, the pressor effects of norepinephrine, angiotensin II, and potassium chloride were all significantly increased when vasopressin was added to the perfusion buffer. Cortisol and lithium both inhibited the potentiating effect of vasopressin but had no effect on the control pressor response to norepinephrine. When the vascular effects of norepinephrine were first blocked with indomethacin and then restored by the addition of prostaglandin E2, the potentiation by vasopressin was almost completely prevented. This suggests that vasopressin may be acting by stimulating prostaglandin biosynthesis. Cortisol and lithium may exert their inhibitory effects by preventing the activation of prostaglandin synthesis by vasopressin. These findings may be of clinical significance because the phenomena occur well within the range of vasopressin levels found in human plasma.

Angiotensin II↗
PubMed1978

The vascular effects of flunarizine as compared with those of other clinically used vasoactive substances.

Flunarizine, a difluoro derivative of cinnarizine, produces a long-lasting inhibition of calcium-induced contractions of isolated vascular preparations of rabbit and rat. In this regard it is slightly more active than cinnarizine and markedly more active than papaverine, naftidrofuryl, bencyclane, cylandelate, dihydroergotoxine, xantinol nicotinate and pentoxifylline; calcium dobesilate does not inhibit the calcium-induced responses. A long-lasting antivasoconstrictor effect was observed also for cinnarizine. This action of flunarizine is selective for calcium channels in vascular tissue, since it has little effect on the calcium-induced response of myocardial preparations of the cat. Flunarizine has no effect on the rhythmic activity of myogenically active blood vessels; it thus shows a further selective activity to calcium channels activated by vasoconstrictor agents and not for those opened by intrinsic changes in membrane permeability. This dual selectivity implies that flunarizine is a useful reference substance in assessing calcium antagonism.

Animals↗