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Renal Prostaglandin Synthesis in ..

Cells having morphological and histochemical properties of collecting tubules were isolated from rabbit renal papillae. Confluent monolayer cultures of these renal papillary collecting tubule (RPCT) cells formed hemicysts and adhered with morphological asymmetry to Millipore filters. Cultures of 1-day-old RPCT cells synthesized cAMP in response to arginine vasopressin (AVP) (half-maximal response at 10-10 M), oxytocin, and parathyroid hormone (half-maximal responses at 5x10-9 M) but not to adrenergic agents. After 10 days of growth (fourfold increase in cell number) RPCT cells retained the same pattern of histochemical and hormonal responses as 1-day-old cells. Hormones were tested for their influence on the release of immunoreactive prostaglandins (iPG) by RPCT cells; the major product under both basal and stimulated conditions was iPGE2. At very low concentrations (≥10-10 M), bradykinin, lysyl-bradykinin, and methionyl-lysyl-bradykinin caused four- to sixfold increases in the rate of iPGE2 formation within 3 min; smaller (-5 M), norepinephrine (10-5 M), and angiotensin II (10-7 M), but only after longer incubations. Significantly, neither AVP (10-7 M) nor [deamino]AVP (10-7 M) caused prostaglandin release by RPCT cells. Our results indicate that kinins can act directly on the collecting tubule to elicit PGE2 formation; furthermore, this effect of kinins may be natriuretic, since PGE2 has been shown to inhibit Na+ resorption by the medullary collecting tubule and thick ascending limb.

T1 - Kinin-induced prostaglandin synthesis by renal papillary collecting tubule cells in culture

N2 - Postnatal development of glomerular filtration rate (GFR) and renal blood flow is associated with a fall in renal vascular resistance that may be mediated by vasoactive substances. We examined differences in the regulation of one such substance, prostaglandin E2 (PGE2). The present studies examined renal cortical and medullary PGE2 synthesis and degradation in rats aged 20 days (30.7 g), 31 days (101 g), and 120 days (413 g). PGE2 synthesis in cortical microsomes was highest in 20-day-old rats compared to 31- and 120-day-old rats. In contrast, medullary PGE2 synthesis was lowest in 20-day-old rats compared to 31- and 120-day-old rats. Both cortical and medullary PGE2 degradation were highest in 20-day-old rats and decreased with age. Despite demonstrating significant age-dependent differences in cortical and medullary PGE2 synthesis, 11 days of aspirin given between age 20-31 days blocked PGE2 synthesis in cortex and medullary by 60 and 76%, respectively, but GFR was similar to control 31-day-old rats (0.78 ± 0.04 ml/min/g kidney weight, aspirin-treated, versus 0.85 ± 0.03 ml/min/g kidney weight, control), suggesting that observed age-dependent differences in renal PGE2 synthesis is not a major determinant of development of GFR. A more important determinant GFR may be age-related differences in renal cortical prostaglandin turnover.

Renal Prostaglandin Synthesis - Vsd Prostaglandin

N2 - Cells having morphological and histochemical properties of collecting tubules were isolated from rabbit renal papillae. Confluent monolayer cultures of these renal papillary collecting tubule (RPCT) cells formed hemicysts and adhered with morphological asymmetry to Millipore filters. Cultures of 1-day-old RPCT cells synthesized cAMP in response to arginine vasopressin (AVP) (half-maximal response at 10-10 M), oxytocin, and parathyroid hormone (half-maximal responses at 5x10-9 M) but not to adrenergic agents. After 10 days of growth (fourfold increase in cell number) RPCT cells retained the same pattern of histochemical and hormonal responses as 1-day-old cells. Hormones were tested for their influence on the release of immunoreactive prostaglandins (iPG) by RPCT cells; the major product under both basal and stimulated conditions was iPGE2. At very low concentrations (≥10-10 M), bradykinin, lysyl-bradykinin, and methionyl-lysyl-bradykinin caused four- to sixfold increases in the rate of iPGE2 formation within 3 min; smaller (-5 M), norepinephrine (10-5 M), and angiotensin II (10-7 M), but only after longer incubations. Significantly, neither AVP (10-7 M) nor [deamino]AVP (10-7 M) caused prostaglandin release by RPCT cells. Our results indicate that kinins can act directly on the collecting tubule to elicit PGE2 formation; furthermore, this effect of kinins may be natriuretic, since PGE2 has been shown to inhibit Na+ resorption by the medullary collecting tubule and thick ascending limb.

AB - Postnatal development of glomerular filtration rate (GFR) and renal blood flow is associated with a fall in renal vascular resistance that may be mediated by vasoactive substances. We examined differences in the regulation of one such substance, prostaglandin E2 (PGE2). The present studies examined renal cortical and medullary PGE2 synthesis and degradation in rats aged 20 days (30.7 g), 31 days (101 g), and 120 days (413 g). PGE2 synthesis in cortical microsomes was highest in 20-day-old rats compared to 31- and 120-day-old rats. In contrast, medullary PGE2 synthesis was lowest in 20-day-old rats compared to 31- and 120-day-old rats. Both cortical and medullary PGE2 degradation were highest in 20-day-old rats and decreased with age. Despite demonstrating significant age-dependent differences in cortical and medullary PGE2 synthesis, 11 days of aspirin given between age 20-31 days blocked PGE2 synthesis in cortex and medullary by 60 and 76%, respectively, but GFR was similar to control 31-day-old rats (0.78 ± 0.04 ml/min/g kidney weight, aspirin-treated, versus 0.85 ± 0.03 ml/min/g kidney weight, control), suggesting that observed age-dependent differences in renal PGE2 synthesis is not a major determinant of development of GFR. A more important determinant GFR may be age-related differences in renal cortical prostaglandin turnover.

JCI - Usage information: Renal prostaglandin synthesis …

AB - Cells having morphological and histochemical properties of collecting tubules were isolated from rabbit renal papillae. Confluent monolayer cultures of these renal papillary collecting tubule (RPCT) cells formed hemicysts and adhered with morphological asymmetry to Millipore filters. Cultures of 1-day-old RPCT cells synthesized cAMP in response to arginine vasopressin (AVP) (half-maximal response at 10-10 M), oxytocin, and parathyroid hormone (half-maximal responses at 5x10-9 M) but not to adrenergic agents. After 10 days of growth (fourfold increase in cell number) RPCT cells retained the same pattern of histochemical and hormonal responses as 1-day-old cells. Hormones were tested for their influence on the release of immunoreactive prostaglandins (iPG) by RPCT cells; the major product under both basal and stimulated conditions was iPGE2. At very low concentrations (≥10-10 M), bradykinin, lysyl-bradykinin, and methionyl-lysyl-bradykinin caused four- to sixfold increases in the rate of iPGE2 formation within 3 min; smaller (-5 M), norepinephrine (10-5 M), and angiotensin II (10-7 M), but only after longer incubations. Significantly, neither AVP (10-7 M) nor [deamino]AVP (10-7 M) caused prostaglandin release by RPCT cells. Our results indicate that kinins can act directly on the collecting tubule to elicit PGE2 formation; furthermore, this effect of kinins may be natriuretic, since PGE2 has been shown to inhibit Na+ resorption by the medullary collecting tubule and thick ascending limb.

Postnatal development of glomerular filtration rate (GFR) and renal blood flow is associated with a fall in renal vascular resistance that may be mediated by vasoactive substances. We examined differences in the regulation of one such substance, prostaglandin E2 (PGE2). The present studies examined renal cortical and medullary PGE2 synthesis and degradation in rats aged 20 days (30.7 g), 31 days (101 g), and 120 days (413 g). PGE2 synthesis in cortical microsomes was highest in 20-day-old rats compared to 31- and 120-day-old rats. In contrast, medullary PGE2 synthesis was lowest in 20-day-old rats compared to 31- and 120-day-old rats. Both cortical and medullary PGE2 degradation were highest in 20-day-old rats and decreased with age. Despite demonstrating significant age-dependent differences in cortical and medullary PGE2 synthesis, 11 days of aspirin given between age 20-31 days blocked PGE2 synthesis in cortex and medullary by 60 and 76%, respectively, but GFR was similar to control 31-day-old rats (0.78 ± 0.04 ml/min/g kidney weight, aspirin-treated, versus 0.85 ± 0.03 ml/min/g kidney weight, control), suggesting that observed age-dependent differences in renal PGE2 synthesis is not a major determinant of development of GFR. A more important determinant GFR may be age-related differences in renal cortical prostaglandin turnover.

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