Canine experiments were designed to determine if both histamine H1 and H2 receptors are present in the renal circulation. Renal blood flow (RBF) increased steeply over the first minute of intra-arterial histamine infusion, then increased gradually to a plateau in 3--5 min. Infusion of either histamine + H2 antagonist or of H1 agonist produced the initial rapid increase in RBF, whereas infusion of either histamine + H1 antagonist or of H2 antagonist produced a slower but more sustained increase in RBF. Histamine significantly increased urine flow rate (V), chloride excretion, and glomerular filtration rate (GFR). Infusion of the H2 agonist also increased V and Cl excretion without affecting GFR. By contrast H1 agonist significantly reduced V and Cl excretion and tended to reduce GFR (P less than 0.1 greater than 0.05). Histamine, H1 agonist, and H2 agonist each increased inner cortical more than outer cortical blood flow. These data suggest that 1) H1 and H2 receptors are present in the renal vasculature, 2) changes in intrarenal blood flow distribution are not responsible for histamine-induced diuresis, and 3) H1 receptors are primarily postglomerular while H2 receptors exhibit both pre- and postglomerular distribution.
1. The effects of myocardial extracts on renal function were studied in the rat. Infusion of rat atrial extract but not of ventricular extract resulted in a significant natriuresis in both pentobarbitone anaesthetized and unanaesthetized rats that were either deprived of food and water (for 18 h before the experiment) or were expanded with isotonic sodium chloride solution (1.5% body weight/h) during the experiment. 2. The increase in sodium excretion was three to four times greater in both groups of volume-expanded rats than in the two groups of food- and water-deprived rats. 3. Glomerular filtration rate and renal blood flow were not affected by atrial extract, indicating that the atrial natriuretic factor (ANF) directly inhibited sodium reabsorption at the tubular level. 4. Distal tubular blockade with a combination of frusemide and amiloride was employed to differentiate between proximal and distal tubular sites of action of ANF. Infusion of atrial extract into saline-expanded, distally blocked rats resulted in a transient increase in both the glomerular filtration rate and sodium excretion; fractional sodium excretion was unaffected by atrial extract in these experiments. 5. We conclude that (a) the renal response to ANF is not affected by pentobarbitone anaesthesia, (b) the renal response to ANF is dependent on the state of the extracellular fluid volume of the animal and (c) that ANF inhibits sodium reabsorption in the distal nephron.
This study was designed to evaluate the renal effects of atrial natriuretic factor [ANF(8-33)] in rats with aminonucleoside (AMN)-induced nephrotic syndrome. AMN (100 mg/kg iv) was administered to adult female rats either 2 (AMN 2, n = 7), 4 (AMN 4, n = 7), 6 (AMN 6, n = 7), or 14 (AMN 14, n = 6) days before clearance experiments; untreated (UNT, n = 7) animals served as controls. During clearance experiments, rats were anesthetized with pentobarbital sodium. Protein excretion rates were similar between UNT and AMN 2 but increased stepwise in AMN 4, AMN 6, and AMN 14 rats. The glomerular filtration rate (GFR) was similar in UNT and AMN 2, lower in AMN 4 and AMN 14, and lowest in AMN 6 rats. Basal sodium excretion (UNaV) was not different among the five groups. An ANF primer (1.0 micrograms/kg iv) plus a constant infusion (0.1 micrograms.kg-1.min-1) for 1 h produced a significantly lower increase in UNaV in AMN 2 and AMN 14 than in UNT and was not natriuretic or diuretic in AMN 4 or AMN 6 rats. The ANF-induced increase in UNaV was similar between AMN 2 and AMN 14 rats. ANF had no effect on the GFR in any group. A higher ANF bolus (5.0 micrograms/kg iv) was then infused. This ANF bolus increased UNaV only in UNT and AMN 2 rats. Finally, a bolus of furosemide (4.0 mg/kg iv) was given; UNaV increased similarly in UNT, AMN 2, and AMN 14, and to a lesser extent in AMN 4 and AMN 6 rats. Thus, there is an attenuated natriuretic and diuretic response to ANF in rats with AMN-induced nephrotic syndrome. This altered responsiveness to ANF may contribute to the sodium and water retention characteristic of this disorder.
The role of histamine (H) and prostaglandins (PGs) in the renal vasoconstriction prompted by a 10-min intrarenal infusion of norepinephrine (NE, 0.2 micrograms), antidiuretic hormone (ADH, 10 mU), or angiotensin II (ANG II, 0.05 micrograms) was evaluated in anesthetized dogs (amounts are per min per kg). Renal blood flow (RBF, flow probe) decreased four- to fivefold during the 1st min of infusion with each agonist but then gradually returned toward base line. This "escape" was greatest with ADH, less with NE, and small with ANG II. There was a postinfusion reactive hyperemia (RH) only after NE; NE-RH was 4.26 +/- 0.75 (SE) ml/g. Meclofenamate (MFA) reduced NE-RH to 60 +/- 11% of control and decreased NE escape. The H1-receptor antagonist, chlorpheniramine (CP), decreased NE-RH to 24 +/- 5% of control and reduced NE escape. MFA slowed, but did not block, ADH escape and had little effect on ANG II escape. CP did not affect ADH or ANG II escape. The histidine decarboxylase inhibitor, p-toluenesulfonohydrazine, did not affect NE escape but decreased NE-RH to 22 +/- 6% of control. Bolus injections of ADH during a constant infusion of the hormone were not vasoactive, indicating a tachyphylaxis-like phenomenon; this was not found with ANG II or NE. Finally, the excretion of histamine-like material increased from a control value of 0.69 +/- 0.08 to 1.28 +/- 0.28 micrograms/min during NE-RH. These results indicate that NE releases histamine and PGs from the kidney and that PGs account, primarily, for NE escape, whereas histamine accounts, primarily, for NE-RH.
We have evaluated the effects of two calcium-channel blockers, verapamil (VP) and manganese (Mn), on endothelin (EN)-induced changes in systemic and renal function in pentobarbital sodium-anesthetized female rats and male and female dogs. In the rat studies, saline was infused at 24 microliters/min iv with or without (n = 10) two doses of VP (0.02 mg.kg-1.min-1, n = 5; 0.03 mg.kg-1.min-1, n = 3) or Mn (0.5 mg.kg-1.min-1, n = 5) throughout the entire experiment. After surgery, rats were allowed 60 min to stabilize, and three 20-min control clearances were collected. EN (100 ng.kg-1.min-1) was then added to the infusate for 30 min. EN alone caused an increase in mean arterial pressure (MAP) and a decrease in the glomerular filtration rate (GFR). VP at either dose and Mn totally blocked the EN-induced increase in MAP. However, the two calcium-channel blockers had no effect on the renal action of EN; the GFR (in ml/min) decreased (at 30 min of EN infusion) from 2.7 +/- 0.1 (SE) to 0.7 +/- 0.1 (P less than 0.01) in controls, from 2.5 +/- 0.3 to 0.4 +/- 0.3 with the lower dose of VP (P less than 0.01), from 2.3 +/- 0.1 to 0.6 +/- 0.2 with the higher dose of VP (P less than 0.01), and from 1.5 +/- 0.5 to 0.9 +/- 0.6 with Mn (P less than 0.05). Infusion of EN alone (10 ng.kg-1.min-1, n = 5) and EN with VP (50 micrograms/min, n = 3) into the renal artery of dogs reduced renal blood flow from 3.5 +/- 0.4 to 0.9 +/- 0.2 and from 3.6 +/- 0.6 to 1.2 +/- 0.6 ml.g-1.min-1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Abstracf. Studies were camed out in 23 anesthetized neonatal dogs aged 2 to 20 days and in 16 adult dogs to compare the effects of saline volume expansion on renal tubular Na and K reabsorption between newborn and adult animals. Proximal-and distal-tubule function was estimated by the distal-nephron-blockade technique using ethacrynic acid and amiloride. During saline infusion, which increased extracellular volume by approximately 30% for both age groups, total nephron fractional Na reabsorption was 0.91 for the adult but 0.98 for the puppy (P < 0.01). However, proximal tubule fractional Na reabsorption was greater in the adult (0.64) than in the puppy (0.48, P < 0.01) whereas distal nephron fractional Na reabsorption was much greater in the newborn (0.5 1) than in the adult (0.26, P < 0.01). Sodium reabsorption normalized to kidney weight was lower in all segments of the neonatal kidney than in the adult kidney. The filtered sodium load was lower in the newborn (27.0 peq min-'g-') than in the adult (105.0, P 23 1
The effects of a natriuretic factor contained in extracts of the atrial myocardium on an isolated renal Na+, K+-ATPase enzyme system were evaluated. Ultrafiltrates (molecular weight < 30,000) of boiled extract of rat atria and ventricles were prepared. Infusion of 100 µl of the atrial ultrafiltrate into bioassay rats resulted in a prompt, short-lived natriuresis and diuresis. However, addition of 100 µl of the atrial ultrafiltrate to 900 µl of a suspension containing Na+, K+-ATPase had no significant effect on enzymatic activity. Similarly, ultrafiltrates of ventricular extract also had no significant effect on Na+, K+-ATPase activity. These results indicate that the atrial natriuretic factor does not alter renal tubular sodium reabsorption by directly inhibiting the Na+, K+-ATPase enzyme system.
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