Renal perfusion pressure is an important determinant of sodium and calcium excretion in DOC-salt hypertension

被引:10
作者
Brands, MW [1 ]
Hall, JE [1 ]
机构
[1] Univ Mississippi, Med Ctr, Dept Physiol & Biophys, Jackson, MS 39216 USA
关键词
DOC-salt hypertension; dog; renal perfusion pressure; sodium; calcium;
D O I
10.1016/S0895-7061(98)00031-4
中图分类号
R6 [外科学];
学科分类号
1002 [临床医学]; 100210 [外科学];
摘要
This study tested the hypothesis that the increased renal perfusion pressure in DOC-salt hypertension is essential for the maintenance of sodium balance and is responsible for the hypercalciuria associated with this model. Twelve chronically instrumented dogs were placed on a high salt intake and mean arterial pressure (MAP) was measured 24 h/day. After a control period, a 17-day DOC infusion period was begun. In six dogs, however, renal perfusion pressure (RPP) to both kidneys was maintained at control levels for the first 12 days of the DOC infusion by the continuous, servo-controlled adjustment of a suprarenal silastic occluder on the abdominal aorta. The servo-controlled dogs had significantly more sodium retention and a greater increase in blood pressure than the six control DOC hypertensive dogs. Urinary calcium excretion in the control dogs began to increase from 24 +/- 6 mg/day on day 1 of DOC, and increased progressively to 100 +/- 14 and 175 +/- 30 mg/day by days 7 and 12, respectively. Plasma ionized calcium decreased, and parathyroid hormone (PTH) (1-84) increased, significantly by day 4. The hypercalciuria was not different in the servo-controlled dogs for the first 7 days of DOC, but was attenuated thereafter. Thus, increased RPP is important in restoring sodium balance and in maintaining the calciuresis in DOC-salt hypertension; however, other mechanisms also are important, particularly during the onset of hypertension. Am J Hypertens 1998;11:1199-1207 (C) 1998 American Journal of Hypertension, Ltd.
引用
收藏
页码:1199 / 1207
页数:9
相关论文
共 27 条
[1]
RENAL DIVALENT-CATION EXCRETION IN SECONDARY HYPERTENSION [J].
BARBAGALLO, M ;
RESNICK, LM ;
SOSA, RE ;
CORBETT, ML ;
LARAGH, JH .
CLINICAL SCIENCE, 1992, 83 (05) :561-565
[2]
VASCULAR SMOOTH MUSCLE - DUAL EFFECT OF CALCIUM [J].
BOHR, DF .
SCIENCE, 1963, 139 (355) :597-&
[3]
ON THE PATHOGENETIC MECHANISM OF HYPERCALCIURIA IN GENETICALLY HYPERTENSIVE RATS OF THE MILAN STRAIN [J].
CIRILLO, M ;
GALLETTI, F ;
STRAZZULLO, P ;
TORIELLI, L ;
MELLONI, MC .
AMERICAN JOURNAL OF HYPERTENSION, 1989, 2 (10) :741-746
[4]
De Vlaming VL., 1977, J FISH BIOL, V10, DOI [10.1111/j.1095-8649.1977.tb04069.x, DOI 10.1111/J.1095-8649.1977.TB04069.X]
[5]
CONCEPT OF NATRIURETIC HORMONE [J].
DEWARDENER, HE ;
CLARKSON, EM .
PHYSIOLOGICAL REVIEWS, 1985, 65 (03) :658-759
[6]
SYSTEMIC AND REGIONAL HEMODYNAMIC-EFFECTS OF DIETARY CALCIUM SUPPLEMENTATION IN MINERALOCORTICOID HYPERTENSION [J].
DIPETTE, DJ ;
GREILICH, PE ;
KERR, NE ;
GRAHAM, GA ;
HOLLAND, OB .
HYPERTENSION, 1989, 13 (01) :77-82
[7]
CELL-MEMBRANE ABNORMALITIES AND THE REGULATION OF INTRACELLULAR CALCIUM-CONCENTRATION IN HYPERTENSION [J].
Dominiczak, AF ;
Bohr, DF .
CLINICAL SCIENCE, 1990, 79 (05) :415-423
[8]
DUARTE CG, 1967, AM J PHYSIOL, V212, P1143
[9]
GONZALEZCAMPOY JM, 1989, KIDNEY INT, V35, P767
[10]
MECHANISMS OF ESCAPE FROM SODIUM RETENTION DURING ANGIOTENSIN-II HYPERTENSION [J].
HALL, JE ;
GRANGER, JP ;
HESTER, RL ;
COLEMAN, TG ;
SMITH, MJ ;
CROSS, RB .
AMERICAN JOURNAL OF PHYSIOLOGY, 1984, 246 (05) :F627-F634