Drugs online research references
Am Fam Physician. 2000 May 15;61(10):3049-56.
Combination antihypertensive drugs: recommendations for use.
Skolnik NS, Beck JD, Clark M.
Abington Memorial Hospital, Jenkintown, Pennsylvania, USA.
The recommendation for first-line therapy for hypertension remains a beta blocker or diuretic given in a low dosage. A target blood pressure of less than 140/90 mm Hg is achieved in about 50 percent of patients treated with monotherapy; two or more agents from different pharmacologic classes are often needed to achieve adequate blood pressure control. Single-dose combination antihypertension therapy is an important option that combines efficacy of blood pressure reduction and a low side effect profile with convenient once-daily dosing to enhance compliance. Combination antihypertensives include combined agents from the following pharmacologic classes: diuretics and potassium-sparing diuretics, beta blockers and diuretics, angiotensin-converting enzyme (ACE) inhibitors and diuretics, angiotensin-II antagonists and diuretics, and calcium channel blockers and ACE inhibitors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10839554&dopt=Abstract
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J Cardiovasc Pharmacol. 1997 Oct;30(4):510-6.
Short-term lisinopril treatment in old rats worsens impairment of angiotensin-induced reflex bradycardia.
Montemayor E, Mellick JR, Kerecsen L, Bunag RD.
Department of Pharmacology, Toxicology, and Therapeutics, College of Health Sciences and Hospital, The University of Kansas Medical Center, Kansas City 66160-7417, U.S.A.
To determine how short-term treatment with an angiotensin-converting enzyme (ACE) inhibitor affects drug-induced reflex bradycardia at different ages in conscious rats, we compared the magnitude of drug-induced reflex bradycardia before and after injecting bolus intravenous doses of lisinopril, 1 mg/100 g, in male Sprague-Dawley rats aged 4 (young) or 19 (old) months. Anesthetic artifacts were avoided by recording all drug-induced cardiovascular responses from femoral arterial cannulas implanted 1 week earlier. For eliciting reflex bradycardia, blood pressure was increased by graded intravenous infusion of angiotensin or phenylephrine. Impairment of reflex bradycardia in old rats occurred only during pressor responses to angiotensin but not when blood pressure was equally increased with phenylephrine. Subsequent administration of lisinopril affected neither pressor and reflex bradycardic responses to phenylephrine nor pressor responses to angiotensin. However, contrary to the baroreflex enhancement described previously by others, the reflex bradycardia induced by angiotensin was reduced by lisinopril treatment but only in old and not in young rats. Thus our results indicate that whereas angiotensin-induced reflex bradycardia was already impaired in old rats before lisinopril was given, it was reduced further after short-term lisinopril treatment.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9335412&dopt=Abstract
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J Hypertens. 1997 Oct;15(10):1151-7.
Actions of angiotensin and lisinopril on thalamic somatosensory neurons in normotensive, non-transgenic and hypertensive, transgenic rats.
Albrecht D, Henklein P, Ganten D.
Institute of Physiology, Faculty of Medicine (Charite), Humboldt University, Berlin, Germany.
OBJECTIVE: To investigate the effects of angiotensin II on discharge rates of somatosensory thalamic neurons and whether these effects are altered in hypertensive transgenic rats [TGR(mREN-2)27] and by long-term treatment with the angiotensin converting enzyme inhibitor lisinopril. DESIGN AND METHODS: Three strains of rats anesthetized with urethane were used (normotensive Wistar and Sprague-Dawley rats (SDR), and [TGR(mREN-2)27]). In addition, the effects of lisinopril treatment on SDR and transgenic animals were tested. The neuronal discharge frequency and the pattern were recorded extracellularly, and their behaviors in response to angiotensin and angiotensin antagonists administered iontophoretically were analyzed. RESULTS: Angiotensin-sensitive neurons located in the ventral posteromedial and ventral posterolateral thalamic nuclei, and in the zona incerta were excited mainly by angiotensin II. The increase in the firing rates induced by administration of angiotensin II often coincided with an increase in the number of bursts of discharges. Effects induced by angiotensin II could be blocked by administration of specific antagonists (losartan, PD 123319). Long-term treatment with lisinopril reduced the neuronal responsiveness to angiotensin II in SDR significantly in comparison with that of untreated SDR controls. Lisinopril-treated SDR had a significantly lower responsiveness to angiotensin II than did hypertensive transgenic rats that had been treated with lisinopril. CONCLUSION: The results show for the first time that administration of angiotensin II induced changes in discharge rates of somatosensory neurons, and that long-term administration of lisinopril caused a significant difference between the neuronal responsiveness to angiotensin of normotensive SDR and that of hypertensive transgenic rats.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9350589&dopt=Abstract
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