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Naunyn Schmiedebergs Arch Pharmacol. 1994 Jun;349(6):627-36.
Arterial contractions induced by cumulative addition of calcium in hypertensive and normotensive rats: influence of endothelium.

Kahonen M, Arvola P, Wu X, Porsti I.

Department of Biomedical Sciences, University of Tampere, Finland.

Responses to cumulative addition of Ca2+ (0.2-2.5 mM) after precontraction with potassium chloride (KCl) and noradrenaline in Ca(2+)-free medium were studied in isolated mesenteric arterial rings from spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). The Ca2+ contractions in 125 mM KCl-stimulated endothelium-denuded rings in the presence of atenolol (10 microM) and phentolamine (10 microM) were less marked in SHR than WKY, although the contractions to high concentrations of KCl in normal organ bath Ca2+ (1.6 mM) were similar in these strains. The difference in Ca2+ contractions between SHR and WKY during KCl stimulation was also present after 10-min pretreatment with 1 mM ethylene glycol bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) in Ca(2+)-free medium. However, when noradrenaline (1 microM) was used as the agonist the Ca2+ contractions of endothelium-denuded rings in the two strains were comparable, while exposure to EGTA reduced these responses more effectively in SHR than WKY. Nifedipine (0.5 nM and 10 nM in KCl- and noradrenaline-stimulated rings, respectively) more efficiently inhibited the Ca2+ contractions in hypertensive than in normotensive rats. The presence of intact vascular endothelium attenuated the contractions to Ca2+ addition comparably (during KCl stimulation) or even more (during noradrenaline) in SHR when compared with WKY. NG-nitro-L-arginine methyl ester (L-NAME, 0.1 mM) counteracted this attenuation correspondingly in WKY and SHR, and L-arginine (1 mM) restored it in both strains, whereas indomethacin (10 mM) was without effect on the response. However, mesenteric arterial relaxations induced by the endothelium-dependent agonists acetylcholine and ADP in noradrenaline-precontracted (1 microM) rings were clearly impaired in SHR, and also L-NAME (0.1 mM) reduced the responses to acetylcholine more efficiently in SHR. In contrast, the relaxations to acetylcholine and ADP in KCl-precontracted (60 mM) rings in the absence and presence of L-NAME were comparable between the two strains. In conclusion, attenuated contractile response to cumulative Ca2+ addition during stimulation with KCl clearly differentiated arterial smooth muscle of hypertensive and normotensive rats, suggesting altered function of cell membrane in SHR. The more pronounced effect of nifedipine on the response indicates abnormal function of voltage-dependent Ca2+ channels, and higher diminishing effect of EGTA on the contraction during noradrenaline suggests exaggerated action of the chelator on membrane-bound Ca2+ in SHR. Interestingly, the depressant effect of intact endothelium on the Ca2+ contraction response, mediated largely via nitric oxide, was not attenuated in SHR.(ABSTRACT TRUNCATED AT 400 WORDS)

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7969514&dopt=Abstract




Circulation. 1994 May;89(5):2401-11.
Vasodepressor reaction induced by inferior vena cava occlusion and isoproterenol in the rat. Role of beta 1- and beta 2-adrenergic receptors.

Waxman MB, Asta JA, Cameron DA.

Department of Medicine, University of Toronto, Ontario, Canada.

BACKGROUND: Testing for the susceptibility of vasodepressor reaction in humans involves the combination of restriction of venous return by passive upright tilting and the administration of isoproterenol. We developed an experimental rat model in which vasodepressor reactions are induced when the inferior vena cava is occluded during an infusion of isoproterenol. The reactions are characterized by the development of paradoxical bradycardia during the period of inferior vena cava occlusion. METHODS AND RESULTS: Inferior vena cava occlusion was performed for 60 seconds, and the maximal changes in RR interval were measured during seven states as follows: (1) when inferior vena cava occlusion was performed under control conditions in 40 rats, the rate accelerated in all 40 rats (delta RR, -15.6 +/- 1.9 milliseconds in 25 rats, P < .001; delta RR, -13.3 +/- 1.7 milliseconds in 10 rats, P < .001); (2) when inferior vena cava occlusion was performed in 25 rats during an infusion of isoproterenol, a vasodepressor reaction was observed in all rats as the heart rate slowed (delta RR, +92.7 +/- 8.3 milliseconds, P < .001); (3) when inferior vena cava occlusion was performed in 10 rats during an infusion of dobutamine, a selective beta 1-agonist, a vasodepressor reaction was observed in all rats as the heart rate slowed (delta RR, +63.3 +/- 10.6 milliseconds, P < .001); (4) when inferior vena cava occlusion was performed in 5 rats during an infusion of salbutamol, a selective beta 2-agonist, vasodepressor reaction was not observed as the heart rate accelerated in all rats (delta RR, -11.4 +/- 2.8 milliseconds, P < .002); (5) the vasodepressor reaction induced by either dobutamine or isoproterenol was inhibited by atenolol, a selective beta 1-adrenergic receptor antagonist; (6) the vasodepressor reaction induced by isoproterenol was inhibited by propranolol (lipophilic) and sotalol (nonlipophilic) beta-blockers and there was a dose-dependent attenuation by propranolol of the maximal RR interval slowing during inferior vena cava occlusion; and (7) butoxamine, a selective beta 2-adrenergic receptor antagonist, attenuated but did not block the vasodepressor reaction observed during an infusion of isoproterenol. CONCLUSIONS: Reduced cardiac volume combined with beta 1-adrenergic stimulation can stimulate a vasodepressor reaction in rats. beta 2-Adrenergic receptors play little or no role in the reaction. The vasodepressor reaction can be blocked by selective or nonselective beta 1-adrenergic antagonists independent of the drug's ability to penetrate the central nervous system. The application of these findings to humans remains to be elucidated.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7910121&dopt=Abstract




Radiology. 1985 Jun;155(3):763-6.
Portal pressure changes induced by medical treatment: US detection.

Zoli M, Marchesini G, Marzocchi A, Marrozzini C, Dondi C, Pisi E.

The portal venous system was studied by ultrasonography (US) in 18 patients with cirrhosis of the liver who had previous bleeding from large esophageal varices. Portal-tract pressure for ten of these patients also was measured by hepatic vein catheterization. After 21 days of treatment with atenolol, the calibers of their splanchnic veins decreased during expiration, while a response to breathing maneuvers was restored. The decrease in the caliber of the splenic and superior mesenteric veins seen by US appeared to correlate significantly with the decrease in portal pressure (P less than .05). Nonresponse to treatment also was detected by US. Real-time US may be routinely carried out as a noninvasive, easy-to-repeat technique for the study of portal system hypertension in patients with cirrhosis undergoing therapy with beta-adrenergic blocking agents.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3890006&dopt=Abstract












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