Vascular actions of furosemide and bumetanide on the rat superior mesenteric vascular bed: interactions with prolactin and prostaglandins

1976 ◽  
Vol 54 (3) ◽  
pp. 357-366 ◽  
Author(s):  
J. P. Mtabaji ◽  
M. S. Manku ◽  
D. F. Horrobin
Keyword(s):  
Pressor Response ◽  
Prostaglandin Synthesis ◽  
Prostaglandin E ◽  
Vascular Effects ◽  
Adequate Amount ◽  
Vascular Bed ◽  
Pressor Responses ◽  
Mesenteric Vascular Bed ◽  
Ovine Prolactin

The mesenteric vascular bed of the rat was used to investigate the effects of furosemide, bumetanide, prolactin, aspirin, indomethacin and prostaglandin E2 on the pressor response to norepinephrine. Furosemide, bumetanide and indomethacin could all inhibit the responses to norepinephrine: in each case responsiveness was restored by the addition of prostaglandin E2 to the perfusate. Bumetanide and furosemide both failed to inhibit responsiveness in the presence of an adequate amount (50 pg/ml) of prostaglandin E2. As has been shown previously, ovine prolactin in a concentration of 50 ng/ml enhanced pressor responses to norepinephrine while 500 ng/ml, after an initial potentiation, inhibited responsiveness. Aspirin, furosemide and bumetanide all reversed both the potentiation produced by the lower prolactin concentration and the inhibition produced by the higher one. When taken in conjunction with other evidence these results suggest that the diuretics exert their vascular effects by inhibiting prostaglandin synthesis whereas prolactin acts by stimulating such synthesis.

Prostaglandin synthetase inhibitors do not decrease hypoxic pulmonary vasoconstriction

1976 ◽  
Vol 41 (5) ◽  
pp. 714-718 ◽  
Author(s):  
E. K. Weir ◽  
I. F. McMurtry ◽  
A. Tucker ◽  
J. T. Reeves ◽  
R. F. Grover
Keyword(s):  
Pressor Response ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Prostaglandin Synthesis ◽  
Pulmonary Vasoconstriction ◽  
Pressor Responses ◽  
Hypoxic Vasoconstriction ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Prostaglandin Antagonists ◽  
The Stability

Prostaglandins are naturally occurring substances with powerful vasoactive effects that are released from tissues during hypoxia or ischemia. Several workers have suggested that a prostaglandin may help to mediate the pulmonary vascular pressor response to alveolar hypoxia. To investigate this possibility, we have measured the pressor responses to hypoxia before and after prostaglandin synthesis antagonism with meclofenamate in eight anesthetized dogs, two groups of awake calves (n=10 and =5), and nine isolated, perfused rat lungs. In addition, synthesis was inhibited by the use of indomethacin in nine additional dogs. The stability of the pulmonary vascular response to repeated hypoxic challenges was demonstrated in nine other dogs. In each species and with both prostaglandin antagonists, the pulmonary pressorresponses to hypoxia were significantly increased rather than reduced. We conclude that prostaglandins do not mediate the pulmonary vasoconstriction caused by hypoxia. The consistent increase observed suggests that hypoxic vasoconstriction stimulates prostaglandin synthesis, the net effect of which is pulmonary vasodilatation which opposes the constriction.

Vasopressin responses and receptors in the mesenteric vasculature of estrogen-treated rats

1986 ◽  
Vol 251 (5) ◽  
pp. H885-H889 ◽  
Author(s):  
J. St-Louis ◽  
A. Parent ◽  
R. Lariviere ◽  
E. L. Schiffrin
Keyword(s):  
Binding Sites ◽  
Pressor Response ◽  
Female Rats ◽  
Maximum Response ◽  
Male Rats ◽  
Ovariectomized Rats ◽  
Binding Characteristics ◽  
Vascular Bed ◽  
Mesenteric Vascular Bed

The effect of treatment with estrogens on the biological activity of arginine8 vasopressin (AVP) in the in vitro perfused mesenteric vascular bed and on the binding characteristics of [3H]AVP on membranes prepared from the same vascular bed was studied. Female rats treated with estradiol (400 micrograms/24 h sc), compared with ovariectomized rats, had an increase in the maximum response to AVP (from 128 +/- 3 to 153 +/- 3 mmHg) in the perfused preparation and an increase in the density of AVP binding sites (from 402 to 732 fmol/mg protein) in the membrane preparation. In male rats, the injection of estradiol increased the maximum response to AVP (from 109 +/- 4 to 137 +/- 3 mmHg) and the density of AVP binding sites (from 289 to 519 fmol/mg protein). The effective concentration producing 50% of maximum response of AVP in the perfused preparation was higher in male than in female rats, while the Kd in the binding experiments was similar in the four experimental groups. Our results show that estrogens upregulate the number of AVP binding sites, leading to an increase in the pressor response to AVP in the rat mesenteric vascular bed.

scholarly journals Role of prostaglandin E in the biphasic fever response to endotoxin

1981 ◽  
Vol 154 (4) ◽  
pp. 1212-1224 ◽  
Author(s):  
RC Skarnes ◽  
SK Brown ◽  
SS Hull ◽  
JA McCracken
Keyword(s):  
Carotid Artery ◽  
Jugular Vein ◽  
Pressor Response ◽  
Arachidonic Acid Metabolism ◽  
Prostaglandin E ◽  
Second Phase ◽  
Plasma Samples ◽  
Arterial Blood ◽  
Pressor Responses ◽  
Fever Response

Biphasic fevers were induced in sheep with intravascular infusions or injections of 4-10 μg (80-200 ng/kg) of endotoxin, whereas monophasic fevers were obtained with doses of 1-2/μg (20-40 ng/kg). A marked increase in arterial blood pressure invariably accompanied the onset of fever; the latency of responses to the higher and lower doses of endotoxins averaged 26 min and 42 min, respectively. Prostaglandin (PG) assays of plasma from the carotid artery and jugular vein during fever episodes revealed a surge of PGE and PGF coincident with the pressor response and the first phase of fever, but PG were not detected in plasma samples taken throughout the second phase of fever. PG measurements of arterial and venous plasma collected at a distal site (hind limb) showed a similar surge of PGE and PGF in association with the early fever response, indicating that intravascular PG synthesis and release represents a generalized systemic response to circulating endotoxin. Carotid arterial infusions of PGE(2) produced immediate monophasic fevers and pressor responses, whereas PGD(2) infusions produced an immediate pressor effect but no fever. Infusions of PGF(2α) or prostacyclin, however, evoked neither fever nor pressor effects. Intracarotid infusions of leukocyte pyrogen (LP) caused monophasic fevers with latent periods of 15-20 min but pressor responses were not seen and neither PGE nor PGF were detected in plasma samples from the carotid artery or jugular vein before or during fever. Indomethacin, a potent inhibitor of arachidonic acid metabolism, blocked fever responses to endotoxin and to LP. These findings implicate PGE as the mediator of the early phase of endotoxin fever and imply a role for another pyrogenic metabolite ofarachidonic acid in the mediation of the second phase of fever, i.e., the phase associated with circulating LP. It is possible that both pyrogenic metabolites are generated within the vascular compartment, reaching thermoregulatory centers of the brain by transfer across the blood-brain interface.

Vascular Actions of Frusemide and Bumetanide on the Rat Superior Mesenteric Vascular Bed: Interactions with Prostaglandins

1976 ◽  
Vol 51 (s3) ◽  
pp. 257s-258s
Author(s):  
D. F. Horrobin ◽  
M. S. Manku ◽  
J. P. Mtabaji
Keyword(s):  
Prostaglandin E2 ◽  
Inhibitory Effect ◽  
Prostaglandin Synthesis ◽  
Inhibitory Effects ◽  
Perfusion Fluid ◽  
Endogenous Prostaglandin ◽  
Vascular Bed ◽  
Mesenteric Vascular Bed

1. The addition of frusemide or bumetanide to perfusion fluid inhibited the response of the isolated mesenteric vascular bed to noradrenaline. 2. Addition of prostaglandin E2 to the perfusion fluid completely restored the response to noradrenaline. 3. Inhibition of prostaglandin secretion by indomethacin with restoration of responses to noradrenaline by the addition of exogenous prostaglandin E2 prevented the inhibitory effect of frusemide or bumetanide on responses to noradrenaline. 4. The inhibitory effects of diuretics on responsiveness to noradrenaline is mediated by blockade of endogenous prostaglandin synthesis.

Disappearance of Angiotensin II and Noradrenaline from the Renal and Femoral Circulations of the Dog

1980 ◽  
Vol 58 (1) ◽  
pp. 29-35 ◽  
Author(s):  
M. J. S. Miller ◽  
G. C. Scroop
Keyword(s):  
Angiotensin Ii ◽  
Renal Artery ◽  
Femoral Artery ◽  
Pressor Response ◽  
Intravenous Route ◽  
Vascular Bed ◽  
Pressor Responses ◽  
Vascular Beds ◽  
Degree Of Extraction ◽  
Renal Vascular

1. The relative ability of the renal and femoral vascular beds to remove infused angiotensin II and noradrenaline was examined in anaesthetized greyhounds. 2. The degree of extraction of infused drug by each vascular bed was expressed as a percentage, calculated by comparing the pressor response to intra-arterial infusion with that obtained when the same dose was administered by the intravenous route. 3. When compared with the same dose given intravenously, the pressor responses after renal artery administration of angiotensin II were reduced by a mean of 77·8 ± 4·1% (mean ± sem, n = 12), whereas those after femoral artery infusions at the same dose were reduced by a mean of only 27·2 ± 4·9%(n = 12). 4. The pattern of extraction seen with noradrenaline infusions administered in a similar manner was the reverse of that with angiotensin II. There was a 28·9 ± 6·8% (n = 7) reduction in pressor responses to renal artery infusions; in contrast, femoral artery infusions of the same dose exhibited a 99·0 ± 1·0% (n = 7) reduction in the pressor responses. 5. Local arterial administration of the angiotensin II competitive antagonist, [Sar1,Ile8]angiotensin II, potentiated the systemic pressor responses to renal artery infusions of angiotensin II, but not those to femoral artery infusions. 6. It is suggested that the marked ability of the renal vascular bed to remove circulating angiotensin II may, in part, involve receptor-binding, although this seems not to be the case in the femoral vascular bed.

Potentiation of Pressor Effects of Noradrenaline and Potassium Ions in the Rat Mesenteric Arteries by Physiological Concentrations of Angiotensin II: Effects of Prostaglandin E2 and Cortisol

1977 ◽  
Vol 53 (3) ◽  
pp. 233-239 ◽  
Author(s):  
K. Kondo ◽  
M. S. Manku ◽  
D. F. Horrobin ◽  
R. Boucher ◽  
J. Genest
Keyword(s):  
Angiotensin Ii ◽  
Prostaglandin E2 ◽  
Potassium Chloride ◽  
Prostaglandin Synthesis ◽  
Mesenteric Arteries ◽  
Potassium Ions ◽  
Vascular Bed ◽  
Vasoconstrictor Response ◽  
Mesenteric Vascular Bed

1. In the perfused rat mesenteric vascular bed, the effects of angiotensin II, cortisol and prostaglandin E2 on the vascular responses to noradrenaline or potassium chloride were studied. 2. Angiotensin II in subpressor concentrations potentiated the vasoconstrictor response to noradrenaline and potassium chloride. This effect of angiotensin II was inhibited in the presence of indomethacin and prostaglandin E2. 3. Cortisol in physiological concentrations inhibited the potentiating effect of angiotensin II. 4. Prostaglandin E2 enhanced the vasoconstrictor response to noradrenaline. This effect was not abolished by cortisol. 5. These results suggest that some actions of angiotensin II and cortisol in vivo are mediated by the regulation of prostaglandin synthesis or release.

Comparative responses to α,β-methylene-ATP in cat pulmonary, mesenteric, and hindquarter vascular beds

2002 ◽  
Vol 93 (4) ◽  
pp. 1287-1295 ◽  
Author(s):  
Trinity J. Bivalacqua ◽  
Hunter C. Champion ◽  
Mrugeshkumar K. Shah ◽  
Bracken J. De Witt ◽  
Edward W. Inscho ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Pyridoxal Phosphate ◽  
Pressor Response ◽  
P2x Receptor ◽  
Disulfonic Acid ◽  
Flow Conditions ◽  
Vascular Bed ◽  
Pressor Responses ◽  
Pressor Activity ◽  
Vascular Beds

Responses to the P2X-purinoceptor agonist α,β-methylene-ATP (α,β-MeATP) were investigated in the pulmonary, hindquarter, and mesenteric vascular beds in the cat. Under constant-flow conditions, injections of α,β-MeATP caused dose-related increases in perfusion pressure in the pulmonary and hindquarter beds and a biphasic response in the mesenteric circulation. In the pulmonary vascular bed, the order of potency was α,β-MeATP > U-46619 > angiotensin II, whereas, in the hindquarters, the order of potency was angiotensin II > U-46619 > α,β-MeATP. The order of potency was similar in the hindquarter and mesenteric beds when the pressor component of the response to α,β-MeATP was compared with responses to angiotensin II and U-46619. The P2X-receptor antagonist pyridoxal-phosphate-6-azophenyl-2′,4′-disulfonic acid attenuated the pressor response to α,β-MeATP in the hindquarter circulation and the pressor component in the mesenteric vascular bed. Pressor responses to α,β-MeATP were not altered by cyclooxygenase, α-adrenergic, or angiotensin AT1 antagonists. These data show that α,β-MeATP has potent pressor activity in the pulmonary circulation, where it was 100-fold more potent than angiotensin II. In contrast, α,β-MeATP had modest pressor activity in the systemic bed, where it was 1,000-fold less potent than angiotensin II. These data suggest that responses to α,β-MeATP are dependent on the vascular bed studied and may be dependent on the density of P2X receptors in the vascular bed.

The influence of phenelzine and tranylcypromine on the release of prostaglandins from the rat mesenteric vascular bed

1988 ◽  
Vol 66 (9) ◽  
pp. 1206-1209 ◽  
Author(s):  
Bassam A. Nassar ◽  
Yung-Sheng Huang ◽  
Alan T. J. McDonald ◽  
Kenneth D. Jenkins ◽  
David F. Horrobin
Keyword(s):  
Arachidonic Acid ◽  
Linolenic Acid ◽  
Inhibitory Effect ◽  
Prostaglandin E ◽  
Low Doses ◽  
Vascular Bed ◽  
Mesenteric Vascular Bed

We investigated the effects of phenelzine and tranylcypromine on the release of prostacyclin, thromboxane A2, prostaglandin E2, and prostaglandin E1 from the isolated perfused rat mesenteric vascular bed. Perfusion of the preparation with phenelzine in concentrations of 15, 45, and 135 μM for 150 min led to attenuated release of all four prostaglandins measured. Inhibition generally occurred with the lowest dose used and was most prominent with the highest concentration. Tranylcypromine also decreased prostaglandin formation. However, low doses were not effective in the suppression of prostacyclin release. Both drugs had an inhibitory effect on production of prostaglandin E1, which is a metabolite of dihomo-γ-linolenic acid, the precursor of arachidonic acid, but this was only shown to be significant with phenelzine. In this work we demonstrate that phenelzine and tranylcypromine have an inhibitory effect on the production of 2-series prostaglandins derived from arachidonic acid, and possibly a similar effect on prostaglandins of the 1-series derived from dihomo-γ-linolenic acid.

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