Drugs online research references
Hypertension. 1995 Dec;26(6 Pt 2):1105-10.
Thyrotropin-releasing hormone hyperactivity in the preoptic area of spontaneously hypertensive rats.
Garcia SI, Dabsys SM, Martinez VN, Delorenzi A, Santajuliana D, Nahmod VE, Finkielman S, Pirola CJ.
Departamento de Sustancias Vasoactivas, Instituto de Investigaciones Medicas A. Lanari, Facultad de Medicina, Universidad de Buenos Aires, Argentina.
Thyrotropin-releasing hormone (TRH) plays an important role in central cardiovascular regulation through the activation of different neurotransmitter systems at distinct extrahypothalamic sites. To study possible alterations in the TRH system in the hypertensive state, we measured TRH concentration in cerebrospinal fluid and TRH content of the preoptic area in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) by radioimmunoassay. In addition, we also measured the density of the TRH receptor in this area by a rapid filtration technique using [3H]methyl-TRH. We found a significant increase in both the TRH content (634 +/- 61 versus 350 +/- 26 pg/mg protein, SHR versus WKY; P < .01, n = 5) and density of TRH receptors without changes in affinity (Bmax, 5.0 +/- 0.1 versus 3.3 +/- 0.1 fmol/mg protein, P < .01, n = 4). An increase in TRH concentration was also found in the cerebrospinal fluid of SHR (30 +/- 3 versus 21 +/- 2 pg/mL, P < .01, n = 5), suggesting increased TRH release in the central nervous system. Northern blot analysis indicated a threefold augmented abundance of TRH precursor mRNA in the preoptic area of SHR. A polyclonal antibody raised against TRH injected peripherally or intracerebroventricularly lowered arterial blood pressure in SHR but not in WKY. In addition, long-term treatment with enalapril (5 mg/kg twice daily), which was effective in inhibiting serum angiotensin-converting enzyme activity by more than 50%, decreased arterial blood pressure and preoptic area TRH content of SHR, whereas another vasodilator, diltiazem (10 mg/kg every 8 hours), failed to produce a similar change.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7498977&dopt=Abstract
Z Kardiol. 1988 Jan;77(1):53-60.
[Regression of hypertensive heart hypertrophy caused by chronic angiotensin-converting enzyme inhibition]
[Article in German]
Motz W, Strauer BE.
Medizinische Einrichtungen der Universitat Dusseldorf, Medizinische Klinik und Poliklinik, Abteilung fur Kardiologie, Pneumologie und Angiologie.
We wanted to determine whether an antihypertensive therapy with the angiotensin-converting enzyme inhibitor enalapril can induce regression of hypertensive hypertrophy. 13 patients with hypertensive left ventricular hypertrophy were treated with enalapril (10-40 mg/day) for 9 months. Left ventricular pump function, left ventricular hypertrophy and geometry were studied by echocardiography before and 3, 6 and 9 months after enalapril treatment had been established. Both a decrease in systolic arterial blood pressure as well as a reversal of myocardial hypertrophy was obtained. After 3 months' therapy, systolic arterial blood pressure dropped from 189 +/- 8 to 171 +/- 9 mm Hg and left ventricular muscle mass decreased from 210 +/- 13 to 196 +/- 8 g/m2. After 6 months' therapy, systolic arterial blood pressure decreased further to 154 +/- 7 mm Hg and left ventricular muscle mass to 181 +/- 8 g/m2. After another 3 months' therapy (after 9 months) no further decrease in systolic arterial blood pressure (159 +/- 9 mm Hg), and no further decrease in left ventricular muscle mass (189 +/- 8 g/m2) were obtained. After 9 months' therapy, reversal of myocardial hypertrophy was adequate in relation to the amount of blood pressure lowering. Due to unaltered ventricular loading conditions, as evidenced by identical systolic wall stress values, left ventricular pump function remained unchanged.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2834885&dopt=Abstract
Am J Med. 1985 Sep 27;79(3C):37-41.
Therapeutic implications of hypertension-induced glomerular injury. Comparison of enalapril and a combination of hydralazine, reserpine, and hydrochlorothiazide in an experimental model.
Raij L, Chiou XC, Owens R, Wrigley B.
Systemic hypertension does not always reflect concomitant glomerular hypertension. At similar levels of systemic hypertension, glomerular injury occurs only in kidneys that lack protective preglomerular vasoconstriction, which results in glomerular hypertension. indeed, glomerular hypertension and glomerular injury do not develop in rats with spontaneous hypertension that have effective preglomerular vasoconstriction. In the experiments reported herein, the normal adaptive response (afferent arteriolar dilation) to a reduction of one and five-sixths of the renal mass in rats with spontaneous hypertension was examined to ascertain whether that response would expose the remaining nephrons to the injurious effects of high perfusion pressure. In addition, the efficacies of two different antihypertensive regimens were compared. Rats with spontaneous hypertension received either no therapy, or a combination of hydralazine, reserpine, and hydrochlorothiazide, or the angiotensin converting enzyme inhibitor enalapril. Three weeks after ablation of one and five-sixths of the renal mass, blood pressure, glomerular filtration rate, urinary protein excretion, and histologic injury scores for mesangial expansion and glomerulosclerosis were determined. Untreated rats with hypertension had severe glomerulosclerosis and mesangial expansion. Both antihypertensive regimens normalized systemic blood pressure and reduced glomerulosclerosis. However, enalapril was more effective than the combination of hydralazine, reserpine, and hydrochlorothiazide in reducing the exaggerated glomerular filtration rate (0.52 +/- 0.40 versus 0.82 +/- 0.10 ml per minute; p less than 0.05), the injury score for mesangial expansion (79 versus 103; p less than 0.05), and the degree of proteinuria (32 +/- 4 versus 42 +/- 3 mg per 24 hours; p less than 0.05). Persistence of hyperfiltration accompanied by increased mesangial expansion, may lead to progression of glomerular damage despite "adequate" control of systemic hypertension, as observed in rats treated with a combination of hydralazine, reserpine, and hydrochlorothiazide.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2996345&dopt=Abstract
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