Abstract
We studied the role of renal papillae in the mechanism of increased sodium excretion during acute increase in mean arterial pressure (MAP). Sodium excretion increased dramatically in normal rats after acute increase in MAP by epinephrine (E) infusion (0.4 ^g/min/100g). Glomerular filtration rate (GFR), renal blood flow (RBF), and papillary plasma flow (PPF) remained unchanged after the E administration. To define the role of the medulla in the mechanism of pressure-induced natriuresis, experiments were performed in a group of rats 8 to 12 days after the development of papillary necrosis induced by bromoethylamine hydrobromide. Urinary sodium and fractional sodium excretions were 2.00 ± 0.34 /iEq/ min and 2.37 ± 0.53% (n = 7), respectively, in papillary necrosis rats infused with saline. Administration of E to papillary necrosis rats, however, failed to increase both urinary sodium (2.89 ± 0.61 /xEq/min) and fractional sodium (FENl, 2.82 ± 0.63%, n = 6) excretions despite a marked increase in MAP (129 vs 150 mm Hg, p < 0.01). The RBF increased slightly after E infusion (4.42 vs 3.24 ml/min/100 g, p < 0.05), but the GFR was not different between the control (0.39 ± 0.05 ml/min/100 g, n = 7) and the Etreated rats (0.43 ± 0.06, n = 6). Failure to increase sodium excretion during acute increase in MAP was not due to the decreased GFR, since control rats with bilateral partial nephrectomy were able to increase sodium excretion from 1.92 ± 0.33to7.76 ± 1.63/xEq/min(p< 0.01) after E infusion. These findings, therefore, suggest that renal papillae play a major role in the mechanism of natriuresis during acute increase in MAP.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 893-898 |
| Number of pages | 6 |
| Journal | Hypertension |
| Volume | 6 |
| Issue number | 6 |
| DOIs | |
| State | Published - Jan 1 1984 |
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Keywords
- Acute hypertension
- Bromoethylamine hydrobromide
- Natriuresis
- Papillary necrosis
- Papillary plasma flow renal papilla
ASJC Scopus subject areas
- Internal Medicine
Cite this
Role of renal papillae in the regulation of sodium excretion during acute elevation of renal perfusion pressure in the rat. / Chen, Pai S.; Caldwell, Robert M.; Hsu, Chen H.
In: Hypertension, Vol. 6, No. 6, 01.01.1984, p. 893-898.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Role of renal papillae in the regulation of sodium excretion during acute elevation of renal perfusion pressure in the rat
AU - Chen, Pai S.
AU - Caldwell, Robert M.
AU - Hsu, Chen H.
PY - 1984/1/1
Y1 - 1984/1/1
N2 - We studied the role of renal papillae in the mechanism of increased sodium excretion during acute increase in mean arterial pressure (MAP). Sodium excretion increased dramatically in normal rats after acute increase in MAP by epinephrine (E) infusion (0.4 ^g/min/100g). Glomerular filtration rate (GFR), renal blood flow (RBF), and papillary plasma flow (PPF) remained unchanged after the E administration. To define the role of the medulla in the mechanism of pressure-induced natriuresis, experiments were performed in a group of rats 8 to 12 days after the development of papillary necrosis induced by bromoethylamine hydrobromide. Urinary sodium and fractional sodium excretions were 2.00 ± 0.34 /iEq/ min and 2.37 ± 0.53% (n = 7), respectively, in papillary necrosis rats infused with saline. Administration of E to papillary necrosis rats, however, failed to increase both urinary sodium (2.89 ± 0.61 /xEq/min) and fractional sodium (FENl, 2.82 ± 0.63%, n = 6) excretions despite a marked increase in MAP (129 vs 150 mm Hg, p < 0.01). The RBF increased slightly after E infusion (4.42 vs 3.24 ml/min/100 g, p < 0.05), but the GFR was not different between the control (0.39 ± 0.05 ml/min/100 g, n = 7) and the Etreated rats (0.43 ± 0.06, n = 6). Failure to increase sodium excretion during acute increase in MAP was not due to the decreased GFR, since control rats with bilateral partial nephrectomy were able to increase sodium excretion from 1.92 ± 0.33to7.76 ± 1.63/xEq/min(p< 0.01) after E infusion. These findings, therefore, suggest that renal papillae play a major role in the mechanism of natriuresis during acute increase in MAP.
AB - We studied the role of renal papillae in the mechanism of increased sodium excretion during acute increase in mean arterial pressure (MAP). Sodium excretion increased dramatically in normal rats after acute increase in MAP by epinephrine (E) infusion (0.4 ^g/min/100g). Glomerular filtration rate (GFR), renal blood flow (RBF), and papillary plasma flow (PPF) remained unchanged after the E administration. To define the role of the medulla in the mechanism of pressure-induced natriuresis, experiments were performed in a group of rats 8 to 12 days after the development of papillary necrosis induced by bromoethylamine hydrobromide. Urinary sodium and fractional sodium excretions were 2.00 ± 0.34 /iEq/ min and 2.37 ± 0.53% (n = 7), respectively, in papillary necrosis rats infused with saline. Administration of E to papillary necrosis rats, however, failed to increase both urinary sodium (2.89 ± 0.61 /xEq/min) and fractional sodium (FENl, 2.82 ± 0.63%, n = 6) excretions despite a marked increase in MAP (129 vs 150 mm Hg, p < 0.01). The RBF increased slightly after E infusion (4.42 vs 3.24 ml/min/100 g, p < 0.05), but the GFR was not different between the control (0.39 ± 0.05 ml/min/100 g, n = 7) and the Etreated rats (0.43 ± 0.06, n = 6). Failure to increase sodium excretion during acute increase in MAP was not due to the decreased GFR, since control rats with bilateral partial nephrectomy were able to increase sodium excretion from 1.92 ± 0.33to7.76 ± 1.63/xEq/min(p< 0.01) after E infusion. These findings, therefore, suggest that renal papillae play a major role in the mechanism of natriuresis during acute increase in MAP.
KW - Acute hypertension
KW - Bromoethylamine hydrobromide
KW - Natriuresis
KW - Papillary necrosis
KW - Papillary plasma flow renal papilla
UR - http://www.scopus.com/inward/record.url?scp=0021688473&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0021688473&partnerID=8YFLogxK
U2 - 10.1161/01.HYP.6.6.893
DO - 10.1161/01.HYP.6.6.893
M3 - Article
C2 - 6519746
AN - SCOPUS:0021688473
VL - 6
SP - 893
EP - 898
JO - Hypertension
JF - Hypertension
SN - 0194-911X
IS - 6
ER -