Drugs online research references
Am J Ther. 1996 Sep;3(9):616-621.
Effects of Terazosin on Glycemic Control, Cholesterol, and Microalbuminuria in Patients with Non--Insulin-Dependent Diabetes Mellitus and Hypertension.
Kirk JK, Konen JC, Shihabi Z, Rocco MV, Summerson JH.
Department of Family and Community Medicine, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, NC, USA.
The use of antihypertensive agents that have positive or neutral effects on blood sugar, lipid profiles, and microalbuminuria can be important clinical treatment for patients with diabetes. We evaluated the effects of both terazosin, a selective alpha-one-adrenergic blocker, and hydrochlorothiazide (HCTZ), a standard mild antihypertensive agent, on glycemic control, urinary albumin excretion rate overnight total cholesterol, and other parameters in non--insulin-dependent diabetes mellitus (NIDDM) patients. A randomized, placebo-controlled, cross-over design was implemented in 25 patients. Over an 8-week treatment period fasting plasma glucose (FPG) and glycosylated hemoglobin (GHgb) improved in the terazosin group. Post-treatment FPG was 200 plus minus 85 and 187 plus minus 71 for patients who received HCTZ and terazosin, respectively. Although the GHgb improved significantly for terazosin patients (12.2 plus minus 5.8 for HCTZ versus 10.7 plus minus 4.6 for terazosin, p = 0.03), microalbuminuria did not improve in terazosin patients in this pilot study. A larger randomized study with tighter blood pressure end points are needed to assess fully the impact of terazosin on micoroalbuminuria and overall glycemic control in the NIDDM patient.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11862301&dopt=Abstract [PubMed - as supplied by publisher]
Hypertension. 2002 Feb;39(2 Pt 2):496-501.
Chronic cardiovascular and renal actions of leptin: role of adrenergic activity.
Carlyle M, Jones OB, Kuo JJ, Hall JE.
Department of Physiology and Biophysics and Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson, MS 39216-4505, USA.
This study was designed to determine the role of changes in adrenergic activity in mediating the chronic cardiovascular, renal, and metabolic actions of leptin. Male Sprague-Dawley rats were implanted with catheters for mean arterial pressure (MAP) and heart rate (HR) measurements and IV infusions of either vehicle (n= 7) or alpha- and beta-adrenergic receptor antagonists, terazosin and propranolol (10 mg/kg/d; n= 8) throughout the study. After control measurements, murine leptin was infused IV (1.0 microg/kg/min) for 7 days along with vehicle or adrenergic antagonists, followed by a 7-day recovery period. Leptin infusion significantly reduced food intake in control rats from 22.6 +/- 0.8 to 10.6 +/- 0.4 g/d and, in adrenergic blockade rats, from 22.6 +/- 0.8 to 13.2 +/- 0.8 g/d. Fasting plasma insulin decreased from 48 +/- 10 to 5 +/- 2 microU/mL in control rats and from 51+/- 9 to 9 +/- 2 microU/mL in adrenergic blockade rats during leptin infusion. Leptin infusion did not significantly alter glomerular filtration rate in either group. MAP and HR increased by 6 +/- 1 mm Hg and 23 +/- 7 bpm after 7 days of leptin infusion in control rats. However, in adrenergic blockade rats, leptin infusion did not significantly alter MAP (-1 +/- 1 mm Hg) and decreased, rather than increased, HR (-23 +/- 8 bpm). These results indicate that leptin-induced increases in blood pressure and tachycardia are mediated by increased adrenergic activity and support the concept that leptin may be an important link between obesity, increased sympathetic activity, and hypertension. However, the chronic effects of leptin on insulin and glucose regulation do not appear to be altered by alpha- and beta-adrenergic receptor blockade.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11882597&dopt=Abstract
Am J Physiol Regul Integr Comp Physiol. 2002 Apr;282(4):R1070-6.
Hypertension in L-NAME-treated diabetic rats depends on an intact sympathetic nervous system.
Fitzgerald SM, Brands MW.
Department of Physiology, Medical College of Georgia, Augusta, Georgia 30912-3000, USA.
We demonstrated previously that induction of diabetes in rats that were treated chronically with the nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) causes a severe, progressive increase in mean arterial pressure. This study tested the role of the sympathetic nervous system in that response. Rats were instrumented with chronic artery and vein catheters and assigned randomly to four diabetic groups pretreated with vehicle (D), L-NAME (D+L), the alpha(1)- and beta-adrenergic receptor antagonists terazosin and propranolol (D+B), or L-NAME, terazosin, and propranolol (D+LB). After baseline measurements were taken, rats were pretreated; 6 days later, streptozotocin was administered and 3 wk of diabetes ensued. D+L rats had a marked, progressive increase in arterial pressure that by day 20 was approximately 60 mmHg greater than in D rats. The pressor response to L-NAME was significantly attenuated in diabetic rats cotreated with adrenergic blockers. During week 1 of diabetes, plasma renin activity (PRA) increased and then returned to control levels in D rats. PRA increased progressively in D+L rats, and chronic adrenergic receptor blockade restored the biphasic renin response in D+LB rats. These results suggest that the sympathetic nervous system may be involved in the hypertensive response to onset of diabetes in L-NAME-treated rats, possibly through control of renin secretion.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11893611&dopt=Abstract
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