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Komatsu K, Numabe A, Ono Y, et al. Hydrochlorothiazide Increases Efferent Glomerular Arteriolar Resistance in Spontaneously Hypertensive Rats. J Cardiovasc Pharmacol Ther. 1996;1(1):57-64doi: 10.1177/107424849600100109.
Komatsu, K., Numabe, A., Ono, Y., & Frohlich, E. D. (1996). Hydrochlorothiazide Increases Efferent Glomerular Arteriolar Resistance in Spontaneously Hypertensive Rats. Journal of cardiovascular pharmacology and therapeutics, 1(1), 57-64. https://doi.org/10.1177/107424849600100109
Komatsu, et al. "Hydrochlorothiazide Increases Efferent Glomerular Arteriolar Resistance in Spontaneously Hypertensive Rats." Journal of cardiovascular pharmacology and therapeutics vol. 1,1 (1996): 57-64. doi: https://doi.org/10.1177/107424849600100109
Komatsu K, Numabe A, Ono Y, Frohlich ED. Hydrochlorothiazide Increases Efferent Glomerular Arteriolar Resistance in Spontaneously Hypertensive Rats. J Cardiovasc Pharmacol Ther. 1996 Jan;1(1):57-64. doi: 10.1177/107424849600100109. PMID: 10684400.
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J Cardiovasc Pharmacol Ther. 1996 Jan;1(1):57-64. doi: 10.1177/107424849600100109.

Hydrochlorothiazide Increases Efferent Glomerular Arteriolar Resistance in Spontaneously Hypertensive Rats.

Journal of cardiovascular pharmacology and therapeutics

Komatsu, Numabe, Ono, Frohlich

Affiliations

  1. Hypertension Research Laboratories, Alton Ochsner Medical Foundation, New Orleans, Louisiana, USA

PMID: 10684400 DOI: 10.1177/107424849600100109

Abstract

BACKGROUND: Micropuncture studies were performed to determine the intrarenal hemodynamic effects of two conventional antihypertensive agents, hydrochlorothiazide (HCTZ) and hydralazine (HYDR) alone and in combination. METHODS AND RESULTS: Male spontaneously hypertensive and normotensive Wistar Kyoto rats (19 weeks old) were treated for 3 weeks with vehicle (control), HCTZ (80 mg/kg/d), HYDR (5 mg/kg/d), or combined therapy (HCTZ 30 mg/kg/d and HYDR 2 mg/kg/d). Each treatment significantly reduced arterial pressure while effective renal plasma flow, glomerular filtration rate and single nephron glomerular filtration rate were unaffected by any treatment in either strain. In spontaneously hypertensive rats HCTZ decreased single nephron plasma flow (111 +/- 8 to 84 +/- 4 nL/min; P <.05) but, despite this reduction, glomerular pressure remained unchanged (51.4 +/- 0.7 to 52.1 +/- 0.8 mmHg) attributable to increased efferent glomerular resistance (1.58 +/- 0.14 to 2.11 +/- 0.12 10 U; P <.05). By contrast, HYDR increased single nephron plasma flow (to 147 +/- 8 nL/min; P <.01) and decreased efferent glomerular resistance (to 1.09 +/- 0.09 U; P <.05). Combined treatment produced responses similar to HCTZ when used alone, thereby nullifying the beneficial efferent glomerular resistance effects: single nephron plasma flow +/- fell (to 89 +/- 7 nL/min; P <.05) and efferent glomerular resistance increased (to 2.05 +/- 0.17 U; P <.05). In Wistar Kyoto rats, HCTZ and combined treatment had no effect. HCTZ alone induced glomerular ischemia that was associated with efferent glomerular arteriolar constriction in these spontaneously hypertensive rats. CONCLUSIONS: These findings provide a possible explanation for the lack of improved renal target-organ damage in controlled multicenter trials employing thiazide diuretics.

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