Vasopressin Stimulates Urinary Kallikrein Excretion in the Isolated Erythrocyte-Perfused Rat Kidney
| Autor: | N B Oza, G W Stephens, Norman G. Levinsky, C. R. Valeri, Wilfred Lieberthal |
|---|---|
| Rok vydání: | 1988 |
| Předmět: |
Calcitonin
Male medicine.medical_specialty Vasopressin Erythrocytes Prostaglandin Antagonists Arginine In Vitro Techniques Kidney Excretion Internal medicine Arginine vasopressin receptor 2 medicine Animals Vasopressin receptor Arginine vasopressin receptor 1B urogenital system Chemistry Hemodynamics Kidney metabolism Rats Inbred Strains General Medicine Rats Arginine Vasopressin Perfusion Endocrinology Parathyroid Hormone Nephrology Renal physiology Scintillation Counting Kallikreins Cardiology and Cardiovascular Medicine hormones hormone substitutes and hormone antagonists circulatory and respiratory physiology |
| Zdroj: | Kidney and Blood Pressure Research. 11:50-59 |
| ISSN: | 1423-0143 1420-4096 |
| DOI: | 10.1159/000173149 |
| Popis: | We have found that arginine vasopressin (AVP) (10 pg/ml) stimulates urinary kallikrein in the isolated erythrocyte perfused rat kidney. (In this model, perfusate flow rate approximates blood flow rates in vivo and morphology is normal.) Urinary kallikrein excretion rose from 6.9 ± 0.8 to 14.9 ± 2.4 ng/min 20 min after the addition of AVP to the perfusate, and then fell towards baseline levels over the next 30 min. 1-Desamino-8-D-AVP (8 pg/ml) caused a comparable increase in kallikrein excretion. Prostaglandin synthesis inhibition with indomethacin did not alter the stimulatory effect of AVP on kallikrein excretion. Parathyroid hormone 1–34 (144 ng/ml) and calcitonin (102 ng/ml) also increased urinary kallikrein. Kallikrein excretion rose from 9.1 ± 2.0 to 24 ± 4.5 ng/min in response to calcitonin and from 8.3 ± 1.6 to 43.7 ± 3.4 ng/min following the addition of parathyroid hormone to the perfusate. Kallikrein was found to accumulate in the perfusate in a linear fashion. Based on the slope of the relationship between perfusate kallikrein and time, the rate of release of kallikrein into the perfusate was estimated to be 0.79 ng/min in control kidneys. The rate of release of kallikrein into the perfusate in kidneys treated with AVP was the same (0.74 ng/min). Thus while kallikrein is released into the perfusate, this process is not influenced by AVP. In conclusion, AVP stimulates release of kallikrein into the urine (but not the perfusate) independently of systemic events. The effect of AVP is not mediated by prostaglandins. This effect of AVP is mediated via stimulation of the V2 receptor and also occurs in response to two other hormones (calcitonin and parathyroid hormone) that are known to stimulate adenyl cyclase in the rat distal nephron. |
| Databáze: | OpenAIRE |
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