Comparison of the Excitatory and Inhibitory Effects of Angiotensin and Vasopressin on Mammalian Portal Vein

Weston, A.H.; Golenhofen, K.

doi:10.1159/000158105

Cited by 8 publications

(9 citation statements)

References 1 publication

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“…In the experiments described here, responses of the muscle membrane to NA, vasopressin and oxytocin also differed with region. In the portal vein, an inhibitory response induced by vasopressin or oxytocin was reported by Carruba et al (1973) and Weston & Golenhofen (1976) but such an inhibition was not observed in the present experiments. This discrepancy is probably due to differences in the concentrations of chlorobutanol added as a preservative.…”

Section: Resultscontrasting

confidence: 55%

Effects of Vasopressin on Smooth Muscle Cells of Guinea‐pig Mesenteric Vessels

Karashima

1981

British J Pharmacology

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1 The effects of vasopressin on the membrane and contractile properties of smooth muscle cells of guinea-pig mesenteric arteries, and mesenteric and portal veins were investigated in various ionic environments by means of a micro-electrode technique and an isometric tension recording method. The results were compared with those obtained with oxytocin and noradrenaline (NA). 2 In the mesenteric jejunal artery, the mean membrane potential was -56.6 + 2.3 mV, s.d, and the membrane was electrically quiescent. Application of outward current pulses generated small graded responses, and the current voltage relationship was linear with application of an inward current pulse. 3 Vasopressin and NA depolarized the membrane and increased the membrane resistance. Vasopressin was a 1000 times more potent than oxytocin in depolarizing the membrane. In high concentrations, vasopressin (1 x 10-3 or 1 x 10-2 iu/ml) or NA (5.9 x 10 5 M) generated slow oscillatory membrane potential changes (slow waves) and spikes during the depolarization. The excitatory actions of vasopressin and NA were not suppressed by tetrodotoxin (3.1 x 10-7 M) or ouabain (1.3 x 10-6 M) and the actions of vasopressin were not suppressed by adrenoceptor blocking agents (3.9 x 10-7 M phentolamine or 3.6 x 10-7 M propranolol). 4 The depolarization induced by vasopressin or NA is mainly due to a decrease in the K-permeability of the membrane. However, the contribution of other ionic species to the depolarization induced by vasopressin or NA differed, e.g. in low concentrations of [Na]o, the NA-induced depolarization was suppressed to a greater extent than that due to vasopressin. In low concentrations of [Ca]o, the vasopressin-induced depolarization was suppressed to a greater extent than with NA.5 In low concentrations of [Ca]. and in the presence of vasopressin or NA, spike generation was inhibited but slow waves were not. In low concentrations of [Na]o, the vasopressin-induced slow waves and spikes were for the great part preserved, but with a high concentration of [Ca]0, vasopressing-induced slow waves were suppressed. 6 Both vasopressin and NA produced contractions in the jejunal mesenteric artery. However, the maximum contraction in response to vasopressin was larger than that to NA, although both induced similar membrane depolarization. In a low concentration of [Na]o, vasopressin but not NA produced a contraction. 7 In the cranial mesenteric artery, NA (5.9 x 10 ) M) depolarized the membrane and produced a contraction, while vasopressin (1 x 10-

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Section: Resultscontrasting

confidence: 55%

Effects of Vasopressin on Smooth Muscle Cells of Guinea‐pig Mesenteric Vessels

Karashima

1981

British J Pharmacology

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“…Furthermore, similarities between this vessel and arterial microvessels have been observed (Ljung, 1970;Grande, 1979). At II induces an increase in AP frequency and a depolarization associated with an increase in contractility in the rat and rabbit portal veins whereas it produces a decrease in electrical and mechanical activity in the guinea-pig portal vein (Weston & Golenhofen, 1976). The purpose of the present study was to investigate further the mode of action of At II on the rat portal vein and more precisely, the mechanism responsible for the acceler-©) Macmillan Publishers Ltd 1982 426 GILLES HAMON & MANUEL WORCEL ation of AP frequency at low concentrations of the peptide, which appear to be more physiologically relevant (Powell-Jackson & MacGregor, 1976).…”

Section: Introductionmentioning

confidence: 98%

Mechanism of Action of Angiotensin Ii on Excitation‐contraction Coupling in the Rat Portal Vein

Hamon¹,

Worcel²

1982

British J Pharmacology

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1 The action of angiotensin II (At II) has been studied on the electrical and mechanical activity of the vascular smooth muscle of the rat portal vein. 2 At low concentrations (between 5 x 10l0 and 10-9 M) At II induces an acceleration of spontaneous action potential (AP) discharge without change in the resting membrane potential. The frequency and size of the associated contractions are simultaneously augmented. Under these conditions the size of the spikes is not affected, thus suggesting that At II triggers the release of Ca2+ from internal stores. 3 The increase in AP discharge rate produced by low concentrations of At II results from an acceleration of the pacemaker potential. Furthermore, in the presence of 10mM tetraethylammonium (TEA), there is an acceleration of the repolarizing phase of AP.4 Ouabain (10-3 M) inhibits the increase in rhythmic activity induced by low concentrations of At II (in the presence of 1OmM TEA), thus suggesting that the Na-K pump is directly or indirectly involved in this action of the peptide. 5 At higher concentrations, At II produces a concentration-dependent depolarization with an EC50 of 1.2 x 10-8M and a maximum of 10-7M. The associated contraction has an EC50 of 3.3 x 10-8 Mand a maximum of 3 x 10-7 M. 6 Ouabain (3 x 10-3 M) depolarizes the cell membrane. Under these conditions, At II (10-7 M) has a slight depolarizing effect, but it still produces a large tonic contraction. 7 It is concluded, that At II acts on different steps of excitation-contraction coupling, depending on the concentration. At low levels, the peptide mainly accelerates spike discharge, through a mechanism involving the Na-K pump. At higher concentrations, At II depolarizes the cell membrane. The contraction is then activated by the influx of Ca2+ due to secondary AP discharge and the release of Ca2+ from intracellular stores. Pharmacomechanical coupling has an important role in the triggering of contractions both at high and at low concentrations of At II.

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“…the literature concerns the inhibitory action of angiotensin II on the guinea pig vein [20] and the absence of stimulatory effects of (a) angiotensin II in the guinea pig vein [3,5] and (b) CER in the rat vein [5,11]. The observed inactivity of CER on the guinea pig vein [5] was perhaps the consequence of less suitable experimental conditions (differ ences in incubation medium containing, e.g., twice as much magnesium sulfate; 31 °C in stead of 37 °C; resting load 1 p instead of 0.5 p).…”

Section: Discussionmentioning

confidence: 99%

Cholecystokinin Octapeptide, Caerulein, Substance P, Neurotensin, and Angiotensin II: Species-Typical Effects on the Isolated Portal Vein of Guinea Pig and Rat

Zetler¹,

Overbeck²

1987

Pharmacology

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The isolated, spontaneously active portal vein of guinea pig was stimulated by the following compounds (the pD₂ is given in parentheses): caerulein (CER, 8.02), cholecystokinin octapeptide (CCK-8, 7.59), substance P (SP, 4.68), and carbachol (5.37), whereas neurotensin (NT) was ineffective and angiotensin II (AII) produced inhibition. On the portal vein of the rat, CER and CCK-8 were ineffective, whereas stimulation occurred with SP (5.72), NT (6.79), AII (7.89), and carbachol (5.50). Tetrodotoxin did not modify these effects in both types of preparation. Cyclic dibutyryl guanosine monophosphate reduced the effect of CCK-8 and CER but not that of carbachol. It is concluded that the peptides stimulate the portal vein in a way independent from intramural neurons. It may be speculated that receptors for CCK-8 and CER are absent in the portal vein of rat and those for NT in the guinea pig vein.

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Comparison of the Excitatory and Inhibitory Effects of Angiotensin and Vasopressin on Mammalian Portal Vein

Cited by 8 publications

References 1 publication

Effects of Vasopressin on Smooth Muscle Cells of Guinea‐pig Mesenteric Vessels

Effects of Vasopressin on Smooth Muscle Cells of Guinea‐pig Mesenteric Vessels

Mechanism of Action of Angiotensin Ii on Excitation‐contraction Coupling in the Rat Portal Vein

Cholecystokinin Octapeptide, Caerulein, Substance P, Neurotensin, and Angiotensin II: Species-Typical Effects on the Isolated Portal Vein of Guinea Pig and Rat

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