Endogenous angiotensin II and the reflex response to stimulation of cardiopulmonary serotonin 5HT3 receptors. Tissue-localized angiotensin II enhances cardiac and renal disorders in Tsukuba hypertensive mice. Effects of angiotensin-converting enzyme inhibitors and sclerotherapy on portal hemodynamics in patients with portal hypertension. Rx drugs

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Br J Pharmacol. 1998 Dec;125(8):1761-7.
Endogenous angiotensin II and the reflex response to stimulation of cardiopulmonary serotonin 5HT3 receptors.

Veelken R, Hilgers KF, Scrogin KE, Mann JF, Schmieder RE.

Department of Medicine-Nephrology, University of Erlangen-Nurnberg, Erlangen, Germany.

1. Angiotensin (Ang) II modulates cardiovascular baroreflexes; whether or not the peptide influences chemosensitive cardiovascular reflexes is not known. We tested the hypothesis that Ang II modulates the reflex control of sympathetic nerve activity exerted by 5-hydroxytryptamine 3 (5HT3) cardiopulmonary receptors. 2. The 5HT3 receptor agonist phenylbiguanide (PBG), infused intravenously for 15 min, elicited a sustained reflex decrease of renal sympathetic nerve activity (RSNA) but only transient (<3 min) changes of arterial blood pressure (BP) and heart rate (HR) in methohexital-anaesthesized rats. 3. Infusion of Ang II at a dose that did not affect baseline BP, HR and RSNA enhanced the PBG-evoked reflex decrease of RSNA (-54+/-5% in Ang II treated versus -33+/-6% in control rats after 15 min PBG, P<0.05, n = 6 each) in methohexital-anaesthetized rats. 4. The angiotensin converting enzyme (ACE) inhibitor lisinopril blunted the reflex responses to PBG in anaesthetized as well as conscious animals. The effect of the ACE inhibitor was abolished by concomitant infusion of Ang II. 5. The reflex response to stimulation of cardiopulmonary 5HT3 afferents was also impaired by the Ang II type 1 receptor (AT1) blocker ZD7155 but not by the type 2 (AT2) blocker PD 123319. 6. Infusion of a volume load to stimulate cardiopulmonary baroreceptors induced a gradual decrease of RSNA which was impaired by exogenous Ang II (RSNA -26+/-6% in Ang II treated versus -47+/-6% in control rats after volume load, P<0.05, n = 6 each) but unaffected by ACE inhibition. 7. The reflex control of RSNA by cardiopulmonary 5HT3 receptors is enhanced by Ang II via AT1 receptors. Thus, Ang II facilitates a chemosensitive cardiovascular reflex, in contrast to its inhibitory influences on mechanosensitive reflexes.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9886768&dopt=Abstract

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J Hypertens. 1998 Dec;16(12 Pt 2):2045-9.
Tissue-localized angiotensin II enhances cardiac and renal disorders in Tsukuba hypertensive mice.

Kai T, Shimada S, Sugimura K, Kurooka A, Takenaka T, Fukamizu A, Murakami K, Ishikawa K.

First Department of Internal Medicine, Kinki University School of Medicine, Osaka-sayama, Osaka, Japan.

OBJECTIVE: To evaluate the relation of tissue-localized angiotensin II (Ang II) concentration with cardiac hypertrophy and glomerulosclerosis in Tsukuba hypertensive mice (THM) carrying both human renin and angiotensinogen genes. DESIGN: Thirty THM aged 12 weeks were distributed equally to a lisinopril dosage group, a hydralazine dosage group, and an untreated group. Ten age-matched C57BL/6 mice were used as normal controls. Administration was performed for 8 weeks from 12 weeks of age. All mice were euthanized at 20 week of age, and the heart-to-body weight ratio, the renal glomerulosclerosis score, tissue Ang II concentration and tissue catecholamine concentration were measured. RESULTS: In the untreated group, a significant increase in every examination item was found as compared with that in C57BL/6 mice. In the lisinopril group, the observed value of every item was significantly lower than that in the untreated group. In the hydralazine group, tissue Ang II and catecholamine concentrations and the heart-to-body weight ratio were not different from those in the untreated group. Although the glomerulosclerosis score in the hydralazine group was significantly less than that in the untreated group, this was significantly higher than that in the lisinopril group. CONCLUSION: Tissue Ang II concentration is more important than hypertension in causing cardiac hypertrophy, and both tissue Ang II level and hypertension are important in causing glomerulosclerosis in THM.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9886895&dopt=Abstract

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Hepatogastroenterology. 2000 May-Jun;47(33):795-806.
Effects of angiotensin-converting enzyme inhibitors and sclerotherapy on portal hemodynamics in patients with portal hypertension.

Nasr AA, el-Hak NG, Settein ME, Khafagy MA, Tadros MT.

Internal Medicine Department, Faculty of Medicine, Mansoura University, Egypt.

BACKGROUND/AIMS: Since pharmacotherapy of portal hypertension has always been a subject of wide interest, we decided to study the effects of different angiotensin-converting enzyme inhibitors and endoscopic sclerotherapy on portal hemodynamics in patients with portal hypertension and bleeding esophageal varices. METHODOLOGY: The study included 72 patients with portal hypertension divided into 6 equal groups. Endoscopic sclerotherapy was done to all patients every 2 weeks for 3 months. In addition, the first 5 groups of patients were maintained on angiotensin-converting enzyme inhibitors for 3 months as follows: group I on perindopril, II on ramipril, III on fosinopril, IV on lisinopril and V on captopril. Portal hemodynamics were determined before and after therapy (using an ultrasonic duplex system). New Doppler portal indices were derived and portal vein kinetic pressure was estimated for the first time by using data derived from the ultrasonic duplex system. RESULTS: 1) Short-term endoscopic sclerotherapy alone resulted in significant elevation of portal vein kinetic pressure, wall stress index and flow volume (P < 0.01) and non-significant increase in the total portal circulation resistance index (P > 0.05) and significantly decreased portal vein compliance and distensibility indices (P < 0.05); 2) Angiotensin-converting enzyme inhibitors reduced the maximum and average portal velocities, the portal flow volume, total portal circulation resistance index and increased portal vein compliance and distensibility indices, hence they reduced the portal vein kinetic pressure significantly in group IV (P < 0.05 for the flow volume and P < 0.01 for other indices); 3) The only side effect encountered was allergic cough (in 8.33% of patients). No effects were noticed on the pulse, systolic, diastolic or mean blood pressures or Child-Pugh Score of liver disease. CONCLUSIONS: 1) Angiotensin-converting enzyme inhibitors when added to endoscopic sclerotherapy can ameliorate the effects of the latter on portal hemodynamics in patients with portal hypertension; 2) Portal vein kinetic pressure, total portal circulation resistance index, portal vein wall stress index, compliance and distensibility indices are new Doppler portal indices that proved to be of value in the follow-up of patients with portal hypertension under sclerotherapy alone or in conjunction with pharmacotherapy; 3) Angiotensin-converting enzyme inhibitors are safe drugs that can be used for portal decompression with endoscopic sclerotherapy. Their use as sole portal anti-hypertensive agents still awaits further studies.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10919035&dopt=Abstract

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