Salt gland blood flow in saltwater-adapted Pekin ducks: Microsphere measurement of the proportionality to secretion rate and investigation of controlling mechanisms

1983 ◽  
Vol 149 (4) ◽  
pp. 457-462 ◽  
Author(s):  
R. Kaul ◽  
R. Gerstberger ◽  
J. -U. Meyer ◽  
E. Simon
Keyword(s):  
Blood Flow ◽  
Salt Gland ◽  
Secretion Rate ◽  
Pekin Ducks

Adrenocortical metabolism of angiotensin in sheep with adrenal transplants.

1978 ◽  
Vol 235 (5) ◽  
pp. E525
Author(s):  
S Lun ◽  
E A Espiner ◽  
D S Hart
Keyword(s):  
Blood Flow ◽  
Adrenal Gland ◽  
Secretion Rate ◽  
Aldosterone Secretion ◽  
Adrenal Tissue ◽  
Rate Analysis ◽  
Venous Plasma

Conscious trained sheep with adrenal gland autotransplants in cervical skin loops were used to study adrenocortical metabolism and clearance of angiotensin (AII) administered by constant systemic infusion. For comparative purposes similar experiments were undertaken in five control sheep with skin loops but no cervical adrenal tissue. During AII infusions (0.33 microgram/min for 30 min), loop venous-arterial AII ratios (0.42--0.62 were similar in both groups of sheep. Measured AII clearances across the skin loop in sheep with and without adrenal transplants were 400--600 and 100--150 pg/min, respectively, which correlated with blood flow (r = 0.79), but showed no relation to aldosterone secretion rate. Analysis of AII immunoreactive fragments showed similar proportions of octa-, hepta-, and hexapeptide fractions (64, 26, and 5%, respectively) in adrenal arterial, adrenal venous, and systemic venous plasma. These studies do not support selective heptapeptide uptake or metabolism by adrenal tissue in vivo and indicate that specific adrenal binding of AII is likely to be less than 400 pg/min at arterial AII concentrations approximating 120 pg/ml.

Effect of arterial carbon dioxide on cerebral blood flow in ducks

1977 ◽  
Vol 232 (6) ◽  
pp. H596-H601 ◽  
Author(s):  
B. Grubb ◽  
C. D. Mills ◽  
J. M. Colacino ◽  
K. Schmidt-Nielsen
Keyword(s):  
Carbon Dioxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Slow Component ◽  
Avian Brain ◽  
Arterial Pco2 ◽  
Pekin Ducks ◽  
Two Component ◽  
Xenon 133

The purpose of this study was to determine the effect of arterial PCO2 on blood flow to the avian brain. Cerebral blood flow was measured on curarized, artificially ventilated Pekin ducks by the rate at which intra-arterially injected xenon-133 was cleared from the duck's brain. A two-component clearance curve resulted: the blood flow calculated from the fast and slow components was similar to the blood flow to mammalian grey and white matter, respectively. Hypercapnia markedly increased the fast component of blood flow, whereas hypocapnia had no effect on this component. These effects were not due to changes in blood pressure, which was independent of arterial PCO2. Blood flow calculated from the slow component was independent of arterial PCO2. We conclude that the lack of response to hypocapnia may contribute to the exceptional tolerance of birds to high altitude by maintaining normal cerebral blood flow.

Intrarenal angiotensin I conversion at normal and reduced renal blood flow in the dog

1983 ◽  
Vol 245 (3) ◽  
pp. F408-F415 ◽  
Author(s):  
L. Rosivall ◽  
D. F. Rinder ◽  
J. Champion ◽  
M. C. Khosla ◽  
L. G. Navar ◽  
...  
Keyword(s):  
Blood Flow ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Formation Rate ◽  
Secretion Rate ◽  
Renin Secretion ◽  
Generation Rate ◽  
Ang Ii ◽  
Angiotensin I ◽  
Single Passage

Intrarenal conversion of angiotensin I (ANG I) to angiotensin II (ANG II) under conditions of normal and reduced renal blood flow (RBF) elicited by constriction of the renal artery was examined in pentobarbital-anesthetized dogs. In eight animals, tracer doses of 125I-ANG I (5-12 pmol) were injected into the renal artery and 125I-ANG I, 125I-ANG II, and 125I-labeled metabolites were measured in renal venous effluent by high-voltage paper electrophoresis. The mean conversion of ANG I to ANG II during a single passage through the kidney was 21.8 +/- 2.1% at control RBF. When RBF was decreased by 25 and 53%, percent ANG I conversion was not altered significantly. In six dogs percent conversion of 125I-[Sar1, Ile5]ANG I, an ANG I analogue refractory to hydrolysis by aminopeptidases, was 18.1 +/- 1.7% at control RBF and did not change significantly when the RBF was reduced by 55%. Although there were severalfold increases in renal renin secretion rate and net ANG I generation rate during reduced RBF, net renal ANG II formation rate did not change significantly. These data indicate that there is substantial conversion of ANG I in a single passage through the dog kidney and that intrarenal ANG I conversion is independent of RBF even under conditions in which renin secretion rate and ANG I generation rate are increased severalfold.

Osmolality and volume factors in salt gland control of pekin ducks after adaptation to chronic salt loading

1979 ◽  
Vol 129 (4) ◽  
pp. 301-308 ◽  
Author(s):  
Hans Deutsch ◽  
Harold T. Hammel ◽  
Eckhart Simon ◽  
Christa Simon-Oppermann
Keyword(s):  
Salt Gland ◽  
Salt Loading ◽  
Pekin Ducks

CORTISOL SECRETION RATE, GLUCOSE ENTRY RATE AND THE MAMMARY UPTAKE OF CORTISOL AND GLUCOSE DURING PREGNANCY AND LACTATION IN DAIRY COWS

1974 ◽  
Vol 62 (2) ◽  
pp. 371-383 ◽  
Author(s):  
J. Y. F. PATERSON ◽  
J. L. LINZELL
Keyword(s):  
Blood Flow ◽  
Milk Yield ◽  
Plasma Cortisol ◽  
Cortisol Concentration ◽  
Secretion Rate ◽  
Cortisol Secretion ◽  
Entry Rate ◽  
Concentration Difference ◽  
Plasma Cortisol Concentration ◽  
Lactating Cows

SUMMARY Glucose entry rate was measured by primed infusion of [2-3H]glucose, and cortisol secretion rate by infusion of [1,2-3H2]cortisol, in two cows from 142 days before calving to day 287 of lactation. Mammary blood flow and the mammary uptake of glucose and cortisol were also measured. In late pregnancy, cortisol secretion rate was 8·6 ± 3·17 (s.d.) μg/min and plasma cortisol concentration was 1·8 ± 0·52 μg/l. During parturition in one animal the secretion rate was 92 μg/min and plasma cortisol concentration was 15 μg/l. During lactation the secretion rate (26·4 ± 7·14 μg/min) and plasma cortisol concentration (5·6 ± 0·73 μg/l) were significantly greater than in dry cows. The mammary uptake of cortisol was 3 to 4% of the secretion rate in both dry and lactating cows. Glucose entry rate was 5·77 ± 2·250 (s.d.) mg/min/kg0·75 in dry cows and there was no significant mammary uptake of glucose. During lactation the glucose entry increased to 9·45 ± 1·881 mg/min/kg0·75. Mammary uptake of glucose was 3·56 ± 1·949 mg/min/kg0·75. The non-mammary utilization of glucose, glucose entry less mammary uptake, was the same for dry and lactating cows. There was a good correlation between glucose entry and milk yield, and between mammary uptake of glucose and milk yield. Since the mammary arterio-venous glucose concentration difference was relatively constant, it is suggested that the change in mammary blood flow may determine the change in glucose uptake and milk yield.

Local inhibition of nitric oxide temporarily stimulates aldosterone secretion in conscious sheep in vivo

2001 ◽  
Vol 280 (4) ◽  
pp. E584-E590 ◽  
Author(s):  
Renato Salemi ◽  
John G. McDougall ◽  
Kenneth J. Hardy ◽  
E. Marelyn Wintour
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Secretion Rate ◽  
Aldosterone Secretion ◽  
Local Inhibition ◽  
Negative Effect ◽  
Endogenous Nitric Oxide ◽  
Conscious Sheep ◽  
Time Point

The effect of localized blockage of endogenous nitric oxide (NO) on basal aldosterone secretion was studied in conscious sheep with autotransplanted adrenal glands. We have shown that infusion of the NO synthase (NOS) inhibitor N G-nitro-l-arginine methyl ester (l-NAME; 130 μg/l blood flow) significantly stimulated basal aldosterone secretion rate (ASR). This stimulatory effect was seen up to 4 h of infusion. Beyond this time point, however, the elevated ASR level was not sustained, and it was seen to drop markedly to lower than control values at 5 h. l-NAME had no effect on cortisol secretion rate (FSR) during the first 4 h of infusion, but a significant reduction in FSR was seen by the 8-h time point. Adrenal blood flow was consistently decreased in association with long l-NAME infusion. Additionally, l-NAME was shown to have no effect on aldosterone secretion when infused systemically. We conclude that the relationship between NO and aldosterone secretion is an inhibitory one, in which NO seems to have a negative effect on basal aldosterone secretion.

Properties of body fluids influencing salt gland secretion in Pekin ducks

1980 ◽  
Vol 239 (5) ◽  
pp. R489-R496
Author(s):  
H. T. Hammel ◽  
C. Simon-Oppermann ◽  
E. Simon
Keyword(s):  
Extracellular Fluid ◽  
Salt Gland ◽  
Colloid Osmotic Pressure ◽  
Threshold Concentration ◽  
Gland Secretion ◽  
Salt Glands ◽  
Control Solution ◽  
Pekin Ducks ◽  
Salt Gland Secretion ◽  
Before And After

Pekin ducks were reared and maintained on 620 mosmol NaCl/kg H2O to enhance the secretory capability of their salt glands. When a control solution of 1,000 mosmol NaCl/kg H2O was infused intravenously at 0.2, 0.4, or 0.6 ml/min for 60-90 min, the infused loads were secreted in approximately equal quantities, indicating that the amount of NaCl in the extracellular fluid (ECF) before and after each infusion did not change. Salt and water secreted in response to experimental infusions of hyposmotic saline or blood were less than the solute and water infused. Thus, ECF volume increased and the Na+ concentration decreased. Infusions of control solution followed these experimental infusions. The salt and water secreted again equaled the amounts infused, indicating that the threshold concentration of Na+ ([Na+]th) for salt gland secretion was decreased by the increase in ECF volume. When the colloid dextran was added to the control solution, its infusion increased the colloid osmotic pressure of the blood and decreased nasal secretion. Because dextran increased the intravascular volume while the interstitial fluid volume (ISFV) decreased, we conclude that the [Na+]th was inversely correlated with ISFV.

cGMP-Mediated Inhibition of cAMP Degradation Stimulates Renin Secretion Without Affecting Renal Hemodynamics.

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 711-711
Author(s):  
Cecilia M Sayago ◽  
William H Beierwaltes
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Direct Effect ◽  
Venous Blood ◽  
Second Messenger ◽  
Renal Hemodynamics ◽  
Secretion Rate ◽  
Renin Secretion ◽  
Before And After

P100 The stimulatory second messenger for renin is cAMP, which is degraded by phosphodiesterase (PDE)-3. PDE-3 is inhibited by cGMP, while PDE-5 degrades cGMP. We hypothesized that if endogenous cGMP was increased, it could inhibit PDE-3, increasing cAMP, and stimulating renin. We used the selective PDE-5 inhibitor Zaprinast at a dose we determined would not change either blood pressure or renal blood flow (RBF). In inactin-anesthetized rats, renin secretion rate (RSR) was determined by collecting arterial and renal venous blood while measuring RBF before and 75 min after administering 20 mg/kg bw Zaprinast (n=9) ip, or vehicle (n=7). Blood pressure before and after Zaprinast was unchanged at 102 ±2 and 98 ±2 mmHg, respectively, similar to vehicle controls (107 ±3 to 105 ±4 mmHg). RBF was unchanged by either Zaprinast (5.57 ±0.38 to 5.77 ±0.41 ml/min/gkw) or vehicle (6.21 ±0.47 to 6.25 ±0.42 ml/min/gkw). Zaprinast increased RSR 6-fold (from 2.95 ±1.74 to 17.62 ±5.46 ng Ang1/hr/min, p <0.024), while vehicle had no effect (4.08 ±2.02 to 3.87 ±1.53 ng Ang1/hr/min). Zaprinast also increased renal cGMP excretion from 12.75 ±1.57 to 18.67 ±1.87 p mol/min (p<0.003), while cGMP excretion was unchanged by vehicle (13.07 ±1.76 to 12.42 ±2.16 p mol/min). Thus, inhibition of cGMP degradation by the PDE-5 inhibitor Zaprinast increased endogenous cGMP (as reflected in excretion) and also stimulated renin secretion, despite not significantly changing renal hemodynamics. These data suggest that endogenous cGMP may indirectly regulate renin through its direct effect on cAMP degradation.

Sign in / Sign up

Export Citation Format

Share Document