Renal micropuncture study of normotensive and Milan hypertensive rats before and after development of hypertension.
Earlier studies of renal transplantation and of sodium metabolism indicated that the cause of high blood pressure in the Milan strain of genetically hypertensive rats (MHS) was altered renal function. To pinpoint the active factors, we used micropuncture to study several indices of renal function in normal (NR) and MHS rats at three different ages: A) 26 to 30 days, before development of hypertension (pre-MHS); B) 35 to 40 days; and C) 75 to 90 days, after the development of hypertension. The indices studied and the important differences found between the two strains were: 1) Single nephron filtration rate (SNFR) and late proximal tubular fluid delivery to the distal nephron (LPF). In group A, the pre-MHS rats had significantly lower values than did the NR (SNFR = 6.3 +/- 0.8 nl/min [MHS] vs. 8.3 +/- 1.2 [NR], P less than 0.01; LPF = 3.14 +/- 0.25 nl/min [MHS] vs. 4.1 +/- 0.35 [NR], p less than 0.05). In group C, the values in the MHS rats were significantly higher than those of the NR (SNFR = 17.3 +/- 1.4 nl/min [MHS] vs. 12.1 +/- 0.8 [NR], P less than 0.05; LPF - 7.4 +/- 0.5 nl/min [MHS] vs. 5.3 +/- 0.3 [NR], P less than 0.01). 2) Number of glomeruli. In group C only, the MHS rats had significantly fewer than did the NR rats (MHS = 55, 253 +/- 2,821 vs. NR = 64,527 +/- 2,900, P less than 0.05). 3) Glomerular filtration rate (GFR) and SNFR as a function of the mean blood pressure (MAP). In group A, the GFR of the MHS rats was lower than that of the NR rats (GFR = 0.38 +/- 0.03 ml/min . 100 g of body wt [MHS], 0.50 +/- 0.03 [NR] P less than 0.05). In group C, there was no longer any significant difference. At equal MAP, SNFR was equal in all the groups, except group A, where SNFR was significantly lower in MHS. 4) Pressure differences: Glomerular capillary pressure (gP). GP was significantly higher in MHS rats than in NR rats (group A, + 5.2 mm Hg; group C, + 6.7 mm Hg). In the pre-MHS rats, anesthesia significantly increased (P less than 0.001) the blood pressure difference between the two strains. This effect was not seen in the adult MHS rats. This may increase the differences in GP between pre-MHS and NR. 5) Afferent effective filtration pressure (EFPA). EFPA values were also higher in MHS rats (+ 2.9 mm Hg in group A, + 6.8 mm Hg in group C), but once again the effects of anesthesia probably account for the differences in magnitude seen between pre-MHS and NR. Only 22% of the absolute differences in systemic arterial pressure in the adult MHS and NR rats was transmitted to the glomerular capillary, while 33% of the difference was transmitted in the younger rats. These values suggest a reduced glomerular hydraulic conductivity, even though other explanations could not be excluded, and they are consistent with the hypothesis that the primary cause of development of hypertension in the MHS rats may be a decrease in SNFR.
D000818:Animals; D001794:Blood Pressure; D001835:Body Weight; D005260:Female; D005919:Glomerular Filtration Rate; D006874:Hydrostatic Pressure; D006973:Hypertension / Q000378:metabolism*; D007668:Kidney / Q000378:metabolism*; D007678:Kidney Glomerulus / Q000098:blood supply; D007686:Kidney Tubules, Distal / Q000378:metabolism; D007687:Kidney Tubules, Proximal / Q000378:metabolism; D009929:Organ Size; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000378:metabolism; D013997:Time Factors; D014867:Water / Q000378:metabolism
D014867:Water; D012964:Sodium