Glomerular dynamics and salt balance in pregnant rats with renal hypertension

1989 ◽  
Vol 256 (4) ◽  
pp. F728-F734 ◽  
Author(s):  
A. Dal Canton ◽  
M. Altomonte ◽  
G. Conte ◽  
C. Esposito ◽  
G. Fuiano ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Hypertension ◽  
Chronic Hypertension ◽  
Marked Rise ◽  
Pregnant Rats ◽  
Hypertension In Pregnancy ◽  
Single Nephron ◽  
Renal Micropuncture ◽  
Glomerular Hemodynamics ◽  
Goldblatt Hypertension

These studies were aimed at investigating whether chronic hypertension in pregnancy causes changes both in salt excretion (NaE) and in glomerular hemodynamics. Metabolic and renal micropuncture studies were performed in pregnant (P) and Virgin (V) Munich-Wistar rats with normal blood pressure (N) and two-kidney Goldblatt hypertension (H). Mean NaE was higher in PN than VN (2.7 vs. 1.7 meq/day, P less than 0.01). Hypertension raised NaE both in P and V rats: in P and V rats with "benign" hypertension (blood pressure less than 180 mmHg) NaE averaged 3.2 and 2.6 meq/day, respectively (P less than 0.05); mean NaE was 5.9 and 3.8 meq/day, respectively (P less than 0.01), in P and V rats with "malignant" hypertension (blood pressure greater than or equal to 180 mmHg). Afferent arteriole resistance (Ra) averaged 1.73 and 3.50 10 dyn.s-1.cm5 in PN and VN, respectively (P less than 0.01). Hypertension raised Ra in V, but not in P rats (4.47 vs. 2.14 10 dyn.s-1.cm5, P less than 0.01). Thus glomerular plasma flow, glomerular capillary hydrostatic pressure, and single-nephron glomerular filtration rate were markedly higher in PH than VH rats: in PH rats single-nephron filtration fraction was significantly lower than in VH. These results show that in PH rats a marked rise in NaE is associated with glomerular vasodilation.

Effects of central and peripheral angiotensin blockade in hypertensive rats

1978 ◽  
Vol 234 (5) ◽  
pp. H629-H637 ◽  
Author(s):  
J. F. Mann ◽  
M. I. Phillips ◽  
R. Dietz ◽  
H. Haebara ◽  
D. Ganten
Keyword(s):  
Blood Pressure ◽  
Renal Hypertension ◽  
Pressure Regulation ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Blood Pressure Decrease ◽  
Different Types ◽  
Angiotensin Blockade ◽  
The Brain ◽  
Goldblatt Hypertension

The angiotensin II (AII) antagonist [Sar1-Ala8]AII (Saralasin) was injected into the brain ventricles (IVT) and intravenously (IV) in five different types of hypertensive unanesthetized rats. Renal hypertension was studied 16-22 days after kidney clipping. Intravenous infusions of cumulative doses (0.1-100 microgram/kg per min) and IVT injections (5-40 microgram) of Saralasin did not change mean arterial pressure (MAP) in controls and in one-clip, one-kidney Goldblatt hypertension, whereas MAP decreased in one-clip, two-kidney Goldblatt hypertension following IV and IVT Saralasin. In two-clip, two kidney hypertensive rats, IVT Saralasin decreased MAP but was ineffective when infused IV. Both IV and IVT Saralasin increased MAP in DOC hypertension. In spontaneously hypertensive (SH) rats, IV Saralasin increased MAP; IVT injection decreased MAP. The effect of IVT Saralasin in SH rats persisted 15-20 h after nephrectomy. We conclude that plasma AII may contribute to peripheral and central mechanisms of blood pressure regulation. The dissociation of the effects of IV and IVT Saralasin and the persistance of blood pressure decrease in nephrectomized SH rats following IVT Saralasin further support a role for locally formed brain angiotensin.

The Vicious Circle in Acute Malignant Hypertension of Rats

1973 ◽  
Vol 45 (s1) ◽  
pp. 251s-255s ◽  
Author(s):  
G. Dauda ◽  
J. Möhring ◽  
K. G. Hofbauer ◽  
E. Homsy ◽  
Ulrike Miksche ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Hypertension ◽  
Plasma Renin ◽  
Malignant Hypertension ◽  
Hypertensive Rats ◽  
Marked Rise ◽  
Contralateral Kidney ◽  
Renal Hypertensive Rats ◽  
Malignant Nephrosclerosis ◽  
Drinking Fluid

1. In renal hypertensive rats, increase in blood pressure above 180 mmHg may induce sodium and water loss, reduced growth rate, elevated haematocrit, a marked rise in plasma renin concentration, an increase in renin extractable from the clamped and the contralateral kidney and malignant nephrosclerosis of the contralateral kidney. These symptoms characterize the malignant phase of renal hypertension in rats. 2. When water was given as drinking fluid, ten of eighteen rats developed signs of malignant hypertension and malignant nephrosclerosis within 3–4 weeks. Administration of 0.9% saline instead of water induced higher blood-pressure levels, but only five of eighteen rats showed malignant nephrosclerosis. When drinking fluid was changed from water to saline shortly before or shortly after the onset of malignant hypertension, the condition improved, and in only one of twelve rats was malignant nephrosclerosis observed. 3. It is concluded that in renal hypertensive rats sodium supplements may improve or prevent signs of malignant hypertension and the development of malignant nephrosclerosis.

Locally produced EDRF controls preglomerular resistance and ultrafiltration coefficient

1993 ◽  
Vol 264 (2) ◽  
pp. F212-F215 ◽  
Author(s):  
A. Deng ◽  
C. Baylis
Keyword(s):  
Blood Pressure ◽  
Glomerular Filtration Rate ◽  
Filtration Rate ◽  
Significant Rise ◽  
Small Reduction ◽  
Renal Vasoconstriction ◽  
Relaxing Factor ◽  
Arterial Blood ◽  
Single Nephron ◽  
Glomerular Hemodynamics

During systemic acute blockade of endogenous endothelial-derived relaxing factor (EDRF) with N-monomethyl-L-arginine (NMA), a significant rise in arterial blood pressure (BP) occurred in the anesthetized rat. Renal vasoconstriction was also seen, with complex changes in glomerular hemodynamics; both preglomerular (RA) and efferent arteriolar (RE) resistances increased, producing a fall in glomerular plasma flow (QA) and a rise in glomerular blood pressure (PGC). The glomerular capillary ultrafiltration coefficient (Kf) was reduced. The net effect was a small fall in single-nephron glomerular filtration rate (SNGFR). To determine the effects of local EDRF blockade, two additional groups were studied with intrarenal administration of NMA; in the first series, one-tenth of the systemic dose was given, which produced no change in BP, a small renal vasoconstriction with an increase in RA, but no change in RE; thus PGC was unaffected. Kf fell, and a small reduction in SNGFR was seen. With a larger intrarenal dose of NMA (one-fifth systemic) a moderate rise in BP occurred, but only RA rose; RE and PGC were unaffected, and Kf and SNGFR fell. These observations suggest that locally produced EDRF controls RA and Kf and that a rise in RE and PGC is only seen with systemic EDRF blockade when a large rise in BP occurs.

scholarly journals The effect of labetalol and nifedipine MR on blood pressure in women with chronic hypertension in pregnancy

2018 ◽  
Vol 11 ◽  
pp. 92-98 ◽  
Author(s):  
E. Shawkat ◽  
H. Mistry ◽  
C. Chmiel ◽  
L. Webster ◽  
L. Chappell ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Chronic Hypertension ◽  
Hypertension In Pregnancy ◽  
In Pregnancy

scholarly journals 22 The effect of labetalol and nifedipine MR on blood pressure in women with chronic hypertension in pregnancy

2016 ◽  
Vol 6 (3) ◽  
pp. 147-148
Author(s):  
Emma Shawkat ◽  
Hitesh Mistry ◽  
Catherine Chmiel ◽  
Edward Johnstone ◽  
Jenny Myers
Keyword(s):  
Blood Pressure ◽  
Chronic Hypertension ◽  
Hypertension In Pregnancy ◽  
In Pregnancy

Chronic exogenous hyperinsulinaemia-induced hypertension in pregnant rats: effect of chronic treatment with l-arginine

2001 ◽  
Vol 100 (6) ◽  
pp. 667-671 ◽  
Author(s):  
Eduardo PODJARNY ◽  
Michael BURSZTYN ◽  
Gloria RASHED ◽  
Sidney BENCHETRIT ◽  
Bernard KATZ ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Risk Factor ◽  
Chronic Treatment ◽  
Blood Pressure Response ◽  
Urinary Metabolites ◽  
Pregnant Rats ◽  
Hypertension In Pregnancy ◽  
Induced Hypertension ◽  
In Pregnancy

Recent studies have shown that maternal hyperinsulinaemia is a risk factor for the development of hypertension in pregnancy. Experimentally, pregnant rats with chronic exogenously induced hyperinsulinaemia (P-INS rats) have increased blood pressure at the end of gestation. This is associated with a blunted elevation of the excretion of the urinary metabolites of nitrate (UNOx). In the present study, we aimed to evaluate the mechanism(s) of the increase in blood pressure in this model. Four groups were studied: normal pregnant rats (P rats), P-INS rats, P-INS rats treated with l-arginine (2 g/l in the drinking water) (l-ARG rats) and hyperinsulinaemic virgin rats (V-INS rats). Systolic blood pressure (SBP), UNOx excretion (on ingestion of a controlled low-nitrate diet), urine noradrenaline (norepinephrine) and plasma endothelin levels were evaluated. Rats were killed on day 22 of pregnancy. Five P-INS rats were not killed at this time, in order to measure SBP 30 and 60 days after delivery. Fetal number and fetal body weight were evaluated. At the end of pregnancy, a 10±3% increase in SBP was found in P-INS rats, contrasting with a fall of -15±4% in P rats (P < 0.01). In the l-ARG group at the end of pregnancy, SBP values had fallen by -14±2%, to values comparable with those of P rats. The increase in UNOx excretion was 175±38% in P rats, 106±12% in l-ARG rats and 41±8% in P-INS rats (P < 0.01 compared with P and l-ARG groups). No differences were found in the urinary excretion of noradrenaline or in the plasma levels of endothelin-1 between the pregnant groups. Fetal number was similar in all groups, but fetal body weight was lower for P-INS rats compared with P and l-ARG rats. Thus the blood pressure response to l-arginine strongly suggests that a decrease in NO availability may be the main pathogenic mechanism involved in the development of hypertension in this model.

Screening for Hypertension in Pregnancy

1992 ◽  
Vol 8 (S1) ◽  
pp. 63-71
Author(s):  
Robert L. Goldenberg
Keyword(s):  
Blood Pressure ◽  
Pregnancy Outcome ◽  
Early Pregnancy ◽  
Chronic Hypertension ◽  
Hypertension In Pregnancy ◽  
Decrease Blood Pressure ◽  
Poor Pregnancy Outcome ◽  
In Pregnancy

AbstractThe literature dealing with screening for hypertension in pregnancy was reviewed. No level of blood pressure or any other factor provides a guarantee of no risk for the development of preeclampsia. However, higher blood pressure in early pregnancy and a failure to decrease blood pressure in midpregnancy are both associated with the development of preeclampsia. The development of proteinuria, rather than the level of blood pressure, is the best predictor of poor pregnancy outcome. Multiparas, especially those with severe chronic hypertension who develop preeclampsia, are at greatest risk of poor pregnancy outcome.

Chronic Hypertension in Pregnancy: New Concepts for Classification and Management

2018 ◽  
Vol 36 (02) ◽  
pp. 161-168 ◽  
Author(s):  
Baha Sibai ◽  
Khalil Chahine
Keyword(s):  
Blood Pressure ◽  
Low Risk ◽  
Chronic Hypertension ◽  
Hypertension In Pregnancy ◽  
New Concepts ◽  
Obstetric Population ◽  
Therapy Target ◽  
Work Up ◽  
In Pregnancy

AbstractChronic hypertension in pregnancy is traditionally classified according to degree of blood pressure (BP) elevation. Alternatively, stratifying women as high or low risk based on the etiology of hypertension, baseline work-up, and comorbid medical conditions will better inform clinicians about thresholds to initiate antihypertensive therapy, target BPs, frequency of antepartum visits, and timing of delivery. Women classified as high-risk chronic hypertension as described here require stricter BP management and more frequent follow-up visits as their associated rates of adverse maternal and/or fetal/neonatal outcomes appear higher than women classified as low-risk chronic hypertension. The latter group can in most cases be managed similarly to the general obstetric population.

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