SEARCH · Search PubMed

Results for “Secretory Rate”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources

PubMed1998

Moderate and large doses of ethanol differentially affect hepatic protein metabolism in humans.

The intake of approximately 70 g of alcohol impairs liver protein metabolism in healthy humans. To establish the threshold at which alcohol impairs hepatic protein metabolism in humans we compared the effects of 500 mL of water (control study), 300 (28.4 g ethanol) or 750 mL (71 g ethanol) of table wine on hepatic protein metabolism in three groups of healthy nonalcoholic volunteers. Hepatic protein metabolism was estimated (L-[1-14C]leucine infusion) by measuring the fractional secretory rates of albumin and fibrinogen during the overnight postabsorptive state (basal) and the subsequent administration of water or two different amounts of wine (300 or 750 mL) given with a liquid glucose-lipid-amino acid meal. During the meal, water did not affect fibrinogen fractional secretory rate and increased albumin fractional secretory rate by approximately 50% (P < 0.01). The 300 mL of wine increased albumin secretory rate by only approximately 20% (P < 0.01 vs. basal, P < 0.04 vs. water) and did not affect fibrinogen secretory rate. The 750 mL of wine profoundly impaired hepatic protein metabolism, decreasing the fractional secretory rates of albumin (P < 0.01 vs. water and 300 mL wine) and fibrinogen (P < 0.04 vs. water and 300 mL of wine) below the postabsorptive values. These results demonstrate that a moderate dose of alcohol (28 g, approximately 2 drinks) slightly affects postprandial hepatic protein metabolism by blunting the meal-induced increase in albumin synthesis, whereas it does not interfere with fibrinogen synthesis as do higher doses.

Adult↗

PubMed1975

Quantitative aspects of insulin secretion and its hepatic and renal removal in sheep.

The secretion of insulin into the portal blood and its removal by the liver and kidneys in conscious fed sheep were determined by simultaneously measuring venoarterial plasma concentration differences and portal, hepatic, and renal plasma flows. The basal secretory rate of insulin was 0.43 +/- 0.03 U/h or 7.8 mU/kg-h. The secretory rate of insulin and the amount of insulin presented to the liver also were altered by 2-h intraportal infusions of glucagon (150 mug/h), insulin (1.17 U/h), and insulin (1.17 U/h) lus glucose (2.2 g/h). Hepatic removal under all conditions was about 50% of the insulin secretory rate, although the extraction ratio was only 0.08. Renal removal was 35% of the insulin secretory rate. The renal extraction ratio was 0.35. During insulin-induced hypoglycemia and also during starvation, the hepatic extraction ratio of insulin increased significantly, but the removal as a percentage of insulin secretion did not change. It appears that in sheep on a maintenance diet the basal secretory rate of insulin is less than that of nonruminant species and that, within physiological limits, the liver disposes of about one-half and the kidney about one-third of the insulin. Other tissues, presumably, remove the remaining 10--20%.

Animals↗

PubMed1979

Bradykinin-induced renal hemodynamic alterations: renin and prostaglandin relationships.

The present studies examined the role of the renin-angiotensin system as a modifier of the renal vasomotor response to bradykinin. Renal arterial bradykinin infusion (80 ng.kg-1.min-1) initially resulted in increased renal blood flow (RBF). The secretory rates of renin and prostaglandins increased after 60 min. With continued bradykinin administration (120 min) RBF and prostaglandin secretory rates returned toward control values, although renin secretory rate remained elevated (P less than 0.02). After prostaglandin synthetase inhibition, RBF decreased and bradykinin administration returned RBF to control values. Prostaglandin secretory rates decreased after meclofenamate (P less than 0.005). Continued bradykinin infusion resulted in a return of the renin secretory rate to control values. The administration of bradykinin after competitive inhibition of angiotensin II resulted in a sustained increase in renal blood flow. These results suggest that the initial bradykinin-induced renal hyperemia is only partially dependent on enhanced prostaglandin release, the increase in renin secretion by bradykinin infusion after prostaglandin synthetase inhibition is consistent with a bradykinin and renin interaction, and the lack of a sustained hyperemia after bradykinin is related to increased renin-angiotensin system activity.

Angiotensin II↗

PubMed1995

The role of gastric histamine release in the acid secretory response to pentagastrin and methacholine in the dog.

We have previously demonstrated that both pentagastrin and methacholine can stimulate histamine release from the canine stomach during short term administration of the secretagogues into the gastrosplenic artery. In this study we tested the hypothesis that gastric histamine release determines the acid secretory response to acid secretagogues. Increasing doses of pentagastrin (2, 6, and 20 ng/kg/min) and methacholine (0.1, 0.3, and 1 micrograms/min) were infused into the gastrosplenic artery in dogs, while gastric acid output, histamine and N tau-methyl histamine secretory rates were monitored. Histamine and N tau-methyl histamine concentrations in plasma were measured using GC/NICI-MS. Increasing doses of pentagastrin resulted in increasing gastric output. Total histamine secretory rate expressed as the sum of histamine and N tau-methyl histamine secretory rate showed a significant increase above basal with the two highest doses of pentagastrin. Regression analysis correlating the dose of pentagastrin to gastric acid output gave a correlation coefficient of 0.586 which was very significant. Regression analysis correlating the total histamine secretory rate to acid output gave a correlation coefficient of 0.498 which was also very significant. Increasing doses of methacholine also resulted in a dose-dependent increase in acid output. Histamine secretory rates showed a statistically significant increase above basal only at the 1 microgram/min infusion rate, however, the total histamine secretory rates (histamine + N tau-methyl histamine) were no longer significant at any of the doses of methacholine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1985

Hyperplastic G cell responsiveness in vitro.

To evaluate the responsiveness of isolated, hyperplastic antral gastrin-producing G cells to a variety of secretagogues, hyperplastic hypergastrinemia was produced in Sprague-Dawley rats by fundusectomy. Mean serum immunoreactive gastrin (IRG) concentration was elevated fivefold above controls 4 days after operation and rose steadily to an eightfold increase at 66 days. Mean antral G cell density remained at control levels for as long as 7 days, increased twofold at 14 days, then remained between twofold and threefold greater than controls for as long as 66 days after operation. Antral mucosa IRG content increased from 141 +/- 38 (control) to 262 +/- 58 ng IRG/gm mucosa (4 to 6 weeks after fundusectomy). Crude fractions of dispersed antral mucosa cells enriched in G cells from fundusectomized rats contained 6.5% +/- 1.4% G cells with 0.19 +/- 0.6 pg IRG/G cell. Corresponding preparations from nonoperated rats contained 5.1% +/- 0.5% G cells with 0.07 +/- 0.02 pg IRG/G cell. Viability averaged greater than 95% for all preparations. Gastrin secretion was monitored in cell preparations further enriched in G cells (9% to 10%) by Percoll density gradient centrifugation either in the absence (basal) or presence of bombesin (1 mumol, 1 nmol/L), carbachol (1 mmol/L), leucine (10 mmol/L), and ethylamine (10 mmol/L). The basal secretory rate of hyperplastic G cell populations averaged 250% greater than normal G cell basal rates. Hyperplastic G cell preparations had an increased IRG secretory rate in the presence of bombesin (1 mumol/L, 750%; 1 nmol/L, 191%), leucine (120%), ethylamine (236%), and carbachol (183%). These conditions failed to increase the IRG secretory rate above basal in preparations from normal antra. Viable, dispersed, hyperplastic G cells have increased IRG content and basal IRG secretory rate and are functionally responsive to a variety of secretagogues.

Animals↗

PubMed1985

Cyclic adenosine 3', 5'-monophosphate levels in human parotid saliva at different secretion rates.

Seventy-four samples of unstimulated and stimulated parotid saliva were collected from 12 healthy male volunteers. The secretion rates and cAMP concentrations were determined. The secretory rate ranged from 0.01 to 1.03 ml/min/gland. The concentration of cyclic AMP varied from 1.6 to 31.9 pmol/ml. The concentration of cAMP was 10.0 +/- 6.5 pmol/ml in unstimulated saliva and 3.8 +/- 1.6 pmol/ml in stimulated saliva. A curvi-linear relationship existed between secretory rate and cyclic AMP concentrations, and the best-fitting regression equation was y = 2.06 + 0.5/x, where y = concentration of cyclic AMP and x = secretory rate.

Adult↗

PubMed1978

The distribution and secretion of kallikrein in some exocrine organs of the rat.

Extractable kallikrein was quantitated in the submandibular, sublingual, and parotid glands and in the pancreas. No kallikrein was detected in the exorbital lacrimal glands and tears. The highest kallikrein concentrations (EU/ml) were in all major salivary gland secretions seen after alpha-adrenergic stimulation, less after beta-adrenergic and least after parasympathetic stimulation. When taking into account the large variations in salivary flow rate, alpha-adrenergic stimulation was in the parotid and particularly in the submandibular gland found to result in the highest kallikrein secretory activity measured by the kallikrein secretory rate(EU/min). This shows that the kallikrein-rich granular tubular cells are selectively activated through alpha-adrenergic sympathetic receptors. The differences observed in the parotid saliva were small and not always statistically significant. However, when cervical nerve stimulation was superimposed upon parasympathetic stimulation, kallikrein secretory rate as well as kallikrein concentration increased. The large individual variations in salivary gland kallikrein content and secretion and the rather small differences observed in kallikrein secretory rate after nervous stimulation of the parotid and sublingual glands, may indicate that the kallikrein-containing striated ducts are also influenced by factors other than the secretory nerves. The kallikrein concentration and secretory rate in urine was studied. A strong positive correlation between kallikrein secretory rate and fluid volume was found in urine but not in saliva.

Animals↗

PubMed1986

Short term memory in the calcium messenger system. Evidence for a sustained activation of protein kinase C in adrenal glomerulosa cells.

If adrenal glomerulosa cells are treated with angiotensin II for a period of 20-30 min, their subsequent response to either a rechallenge with the same concentration of angiotensin II or treatment with BAY K 8644, a calcium channel agonist, differs from the responses of control cells. Perifusion of control cells with 10 nM-angiotensin II leads to an increase in aldosterone secretory rate from 44 +/- 7 to 166 +/- 9 pg/min per 10(6) cells, but perifusion of cells pretreated for a 20 min period with angiotensin II leads to an increase in secretory rate from 51 +/- 9 to 209 +/- 18 pg/min per 10(6) cells. Likewise, treatment of control cells with 10 nM-BAY K 8644 leads to no significant increase in aldosterone secretory rate, but treatment of previously exposed cells to angiotensin II leads to an increase in rate from 51 +/- 9 to 130 +/- 11 pg/min per 10(6) cells. This memory effect is time-dependent in two ways: cells must be exposed to angiotensin II for 20 min or more before it is apparent; the longer the time between removal of angiotensin II and the rechallenge, the less effect these agents have on aldosterone secretory rate. When cells are exposed to angiotensin II for 20 min and then treated with [Sar1,Ala8]angiotensin II, a competitive antagonist of angiotensin II action, the aldosterone secretory rate falls to basal with a half time of 5-7 min. If BAY K 8644 is added simultaneously with [Sar1,Ala8]angiotensin II, the secretory rate falls with a halftime of 35-60 min. BAY K 8644 increases Ca2+ influx rate to the same extent in the presence or absence of [Sar1,Ala8]angiotensin II, and does not alter the effect of either angiotensin II or [Sar1,Ala8]angiotensin II on the production of inositol tris-, bis-, or mono-phosphate. In cells treated with 10 nM-angiotensin II for either 20, 30 or 45 min, the extent of phosphorylation of four cellular proteins is increased. If cells treated for 20 min with angiotensin II are then treated with [Sar1,Ala8]angiotensin II, and examined 15 min later (35 min), there is no longer an increase in the extent of phosphorylation of any of the four proteins. If such cells are then treated with 10 nM-BAY K 8644 and re-examined 5 min later (40 min), all four patients show an increase in the extent of phosphorylation.(ABSTRACT TRUNCATED AT 400 WORDS)

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed1983

Comparison of the effects of rubidium and potassium on renin secretion from rat kidney slices.

It has been shown previously that both low (less than 2 mM) and high (greater than 45 mM) concentrations of extracellular K inhibit the renin secretory rate of rat kidney slices, and that nonidentical Ca-dependent mechanisms appear to be involved. As Rb can substitute for K in many biological systems, the present experiments were designed to compare the effects of K and Rb on renin secretion of rat kidney slices. Adding either KCl or RbCl to a nominally K-free incubation medium stimulated renin secretory rate in concentration-dependent manners; secretory rate was half-maximally stimulated at approximately 1.5 mM and maximally stimulated at approximately 2-3 mM concentrations of either KCl or RbCl. Ouabain completely abolished the basal secretory rate, in either KCl- or RbCl-containing media. These results suggest that the effects of increasing KCl or RbCl in the range of 0.5-4 mM are attributable to stimulatory effects of Rb and K on Na-K-ATPase activity. Renin secretory rate was greatly inhibited by incubating kidney slices in media containing 60 mM concentrations of either KCl or RbCl. A concentration of methoxy-verapamil which completely blocked the inhibitory effects of 60 mM KCl or of 60 mM RbCl failed to antagonize the inhibitory effects of a nominally K-free medium or of media containing ouabain and either 4 mM KCl or 4 mM RbCl. Taken together with previous results, these observations suggest that Rb can substitute for K in the renin secretory process. Furthermore, they support the hypothesis that inhibitors of Na-K-ATPase, and depolarization inhibit renin secretion by Ca-dependent mechanisms which are not identical.

Animals↗

PubMed1988

Peripheral insulin parallels changes in insulin secretion more closely than C-peptide after bolus intravenous glucose administration.

The changes in peripheral serum insulin and plasma C-peptide levels and in the insulin secretory rate in response to iv glucose (0.5 g/kg BW) administration were studied in seven normal subjects. Insulin secretory rates were calculated according to a two-compartment model of distribution for C-peptide, using individual C-peptide kinetics calculated from iv bolus injections of biosynthetic human C-peptide. The mean plasma glucose level increased from a fasting level of 5.1 +/- 0.1 (+/- SE) to a peak of 24.0 +/- 1.0 mmol/L at 3 min and reached basal levels 101 +/- 6 min after glucose administration. The mean serum insulin value increased from 50 +/- 12 to a peak of 405 +/- 58 pmol/L at 3 min and then declined to fasting levels 139 +/- 14 min after the stimulus. In contrast, the mean plasma C-peptide level increased from 390 +/- 50 to a peak of 1460 +/- 210 pmol/L at 3 min and only began declining 45 min after glucose administration, reaching fasting levels 191 +/- 15 min after the stimulus. The mean insulin secretory rate increased from 69.8 +/- 19.9 to a peak of 1412.7 +/- 159.1 pmol/min at 3 min (15.3 +/- 2.5-fold elevation over baseline) and reached basal levels 135 +/- 12 min after the stimulus. The clearance of endogenous insulin during the basal period (2.505 +/- 0.365 L/min) and that during the 4 h after the stimulus (2.319 +/- 0.230 L/min) were similar. In conclusion, after bolus iv glucose administration: 1) the insulin secretory rate is more closely represented by changes in peripheral serum insulin than in plasma C-peptide levels; and 2) no change in endogenous insulin clearance occurs.

Adult↗

PubMed1977

In vitro measurement of rate of fluid secretion in rat isolated seminiferous tubules: effects of metabolic inhibitors and ions.

1. An in vitro technique for measuring secretory rate in rat isolated seminiferous tubules is described. 2. The basal rate of fluid secretion was 0-44+/-0-06 nl. cm-1 min-1 (S.E.) (n=21). The rate was found to be inhibited by cooling, addition of metabolic inhibitor 2,4-dinitrophenol (2-5 x 10(-4) M) and removal of glucose from the incubating solution. This indicates that fluid secretion in isolated rat seminiferous tubules is an energy dependent process. 3. Removal of K+ from the incubating medium inhibited the secretory rate in the isolated seminiferous tubules, whereas a fivefold increase in [K+]0 to 23-5 mM had no effect. The secretory rate was also unaffected by the absence of Cl- in the peritubular fluid. 4. Removal of Ca2+ from the peritubular medium caused a rise in the secretory rate. 5. Ouabain (10(-3) M) and acetazolamide (4 x 10(-5) M) caused a fall in the rate of fluid secretion in isolated seminiferous tubules. 6. These results are discussed in relation to the nature of the ionic secretion produced in the tubules.

Acetazolamide↗

PubMed1976

[On the significance of beta-adrenergic stimuli for the gastric secretion in humans].

In adults of both sexes, the influence on the basal and the maximal by means of pentagastrin stimulated gastric secretion of a single intravenous injection of 8 mg (0.09 to 0.16 mg/kg) oxyfedrine or of two intramuscular injections of 1 mg (0.014 to 0.016 mg/kg) or of 2.5 mg (0.033 to 0.045 mg/kg) in each case isoproterenol, consecutively administered at an interval of 15 minutes, was studied. At a dose which evokes cardiovascular responses isoproterenol does not produce a significant change of the secretory rates of H+, C1-, Na+, K+, Ca++ and Mg++ or of the ionic composition of gastric juice both during basal and maximal acid output. Oxyfedrine shows only during maximal acid stimulation some effects on gastric secretion: a significant rise of the concentration and secretory rate of H+ and of the secretory rate of C1- and a significant decline of the concentration of Na+ and of both the concentration and secretory rate of Mg++. Beta-adrenergic receptors seem not to play any part in the regulation of the production of gastric juice. Possibly, the action of oxyfedrine on the stimulated gastric mucosa may be mediated by a stimulation of alpha-adrenergic receptors or by inhibition of the activity of 3',5'-AMP-phosphodiesterase.

Adrenergic beta-Agonists↗

PubMed1971

Stimulation of amylase secretion from the perfused cat pancreas by potassium and other alkali metal ions.

1. In the isolated cat pancreas, stimulated maximally with secretin, increasing the perfusate potassium concentration (at the expense of sodium ions) caused a copious secretion of amylase from the gland, reduced the volume rate of secretion and caused vasoconstriction.2. Rubidium and caesium had similar effects to potassium: lithium, though depressing secretory rate, had no effect on enzyme secretion or vasoconstrictor action.3. Amylase secretion was detected at potassium concentrations of 30 mM and was maximal at 80-90 mM, output declining as the concentration was raised to 120 mM.4. Amylase secretion was maximal during the first few minutes of exposure to excess potassium, but remained above basal levels throughout the test period. Secretory rate was depressed by a constant amount during the test period.5. Atropine sulphate blocked the effect on enzyme secretion without affecting the reduction in secretory rate.6. During perfusion with excess potassium a vasodepressor material with the properties of acetylcholine was detected in the effluent from the gland.7. The reduction in secretory rate, when perfusate sodium was replaced by potassium, was equal to that obtained when sodium was replaced by sucrose.8. It is concluded that potassium stimulates amylase secretion indirectly by releasing acetylcholine from nerve terminals in the gland, and that the reduction in secretory rate is due not to excess potassium but to sodium deficiency.

Acetylcholine↗

PubMed1984

The anionic basis of fluid secretion by the rabbit mandibular salivary gland.

The role played by anions in salivary secretion has been studied in experiments on the isolated, perfused mandibular gland of the rabbit, in which perfusate Cl- and/or HCO3- were replaced by other anions. Replacement of Cl- with Br- had no significant effect on salivary secretion rate, but replacement with the other anions tested caused secretory rate to fall, by 38% (I-), 50% (NO3-), 61% (isethionate, ise -), and 66% ( CH3SO4 -), respectively. Replacement of perfusate Cl- with ise - or CH3SO4 - caused the salivary HCO3- concentration to rise up to 4-fold. Replacement with Br- or I- seemed to have little effect on salivary HCO3- concentration but, in contrast to ise -, Br- and I- entered the saliva in concentrations comparable to those of Cl- during control perfusion. In glands perfused with HCO3- and ise -, the addition of methazolamide, an inhibitor of carbonic anhydrase, caused a further 60% drop in secretory rate, but the saliva remained rich in HCO3-. Replacement of perfusate HCO3- with Cl- or ise - had no effect on salivary secretion or composition. Replacement of both HCO3- and Cl- in the perfusate with ise - reduced salivary secretion to less than 2% of control levels. In control glands (i.e. perfused with both HCO3- and Cl-), administration of furosemide, an inhibitor of Na+/Cl- co-transport, reduced the secretion rate and increased salivary HCO3- in a manner indistinguishable from that seen when perfusate Cl- was replaced with ise -. In control perfused glands, administration of SITS (4-acetamido-4'- isothio cyano-2,2'-disulphonic acid stilbene), an inhibitor of Cl-/HCO3- antiports , did not cause any change in salivary HCO3- concentration. Unexpectedly, it induced a significant increase in salivary secretory rate. The results show that salivary secretion depends on two independent transport systems. One is a Cl- -dependent, furosemide-sensitive system, probably a Na+/Cl- symport. The other is an HCO3- -dependent, methazolamide-sensitive system, and is probably an Na+/H+ antiport.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗

PubMed1981

Calcium dependency of the inhibitory effect of antidiuretic hormone on in vitro renin secretion in rats.

1. Synthetic arginine-vasopressin (ADH or antidiuretic hormone) inhibited renin secretory rate of rat renal cortical slices. The response was concentration-dependent and was maximal at 0.1 U . ml.-1. 2. Ca depletion (incubation of slices in medium containing Na2EGTA and no added CaCl2) stimulated renin secretion and eventually abolished the inhibitory effect of ADH. Both these effects were reversible. 3. The Ca antagonist D-600, at 0.5 microM, reversed the inhibitory effect of K depolarization on secretory rate but had no effect on secretory rate on on-depolarized slices. In the presence of 0.5 microM-D-600, ADH inhibited the secretory rate of either depolarized or non-depolarized slices. 4. These results confirm and extend previous observations suggesting that Ca plays an inhibitory coupling role in the control of renin secretion. Moreover they suggest that although Ca influx through voltage-sensitive Ca channels influences the secretory activity of juxtaglomerular cells, ADH activates an independent pathway for Ca mobilization.

Animals↗

PubMed1992

The role of gastric secretagogues in regulating gastric histamine release in vivo.

The effect of short-term intragastric arterial infusion of pentagastrin and methacholine on histamine and N tau-methyl histamine secretory rates was evaluated in mongrel dogs in vivo. Doses of pentagastrin and methacholine were chosen that stimulate gastric acid secretion equivalently. Histamine and N tau-methyl histamine secretory rates were evaluated by measuring the arterial and gastric venous plasma histamine and N tau-methyl histamine concentrations at several time points during the secretagogue infusion, and gastric blood flow was continuously monitored. Histamine and N tau-methyl histamine plasma concentrations were analyzed by stable isotope dilution technique using gas chromatography/negative ion-chemical ionization mass spectrometry. Histamine and N tau-methyl histamine secretory rates were calculated by subtracting the arterial from the venous plasma concentrations and multiplying the difference by gastric plasma flow. Infusion of pentagastrin resulted in large pulsed increase of histamine release from 1.5 +/- 0.7 ng/min at time 0 to 72 +/- 20 ng/min at 5 minutes, which decreased to a plateau of 20 +/- 8 ng/min at 20 minutes. N tau-Methyl histamine secretory rate increased from 6.7 +/- 1.9 ng/min at baseline to a maximum of 42.5 +/- 13.1 ng/min at 10 minutes, and the increase was maintained for the duration of the pentagastrin infusion. Methacholine infusion was associated with a small but sustained increase in histamine release, from a baseline of 1.6 +/- 0.6 ng/min to 5.9 +/- 1.7 ng/min at 5 minutes. N tau-Methyl histamine secretory rate was unchanged by methacholine. Gastric blood flow changes to pentagastrin roughly paralleled the extent of histamine release, but methacholine is a gastric vasodilator in its own right. Our data indicate that pentagastrin is a much more effective stimulator of gastric histamine release than methacholine and that the overall role of histamine in gastrin-stimulated acid output is likely to be different from the role of histamine in cholinergic-mediated gastric acid output.

Analysis of Variance↗

PubMed1983

Comparative in vitro responses of fetal, pregnant and non-pregnant rabbits' adrenal glands to steroidogenic agents.

The in vitro secretion of aldosterone and corticosterone by the adrenal glands of fetal (day 30), pregnant and non-pregnant rabbits was examined under basal and stimulated conditions. In general, non-pregnant animals basally secreted less aldosterone than either pregnant or fetal rabbits, whereas basal corticosterone secretion by pregnant animals exceeded that of either fetal or non-pregnant animals. At similar doses of adrenocorticotropin (ACTH), fetal and pregnant adrenal glands produced comparatively more aldosterone than non-pregnant animals, while corticosterone secretion was accelerated to a greater degree in fetal rabbits than in the other groups. Angiotensin II had its greatest effect on the aldosterone secretory rates of fetal and non-pregnant animals without affecting corticosterone secretion in any group. Elevated potassium (K+) enhanced the secretory rates of aldosterone and corticosterone in fetal animals, while increasing only aldosterone secretion in non-pregnant rabbits. Serotonin accelerated aldosterone secretion in all animals, whereas it increased corticosterone secretion only in non-pregnant animals. These results suggest that (1) in fetal rabbits, the secretory rates of both aldosterone and corticosterone are regulated primarily by ACTH and to a much lesser extent by angiotensin II and K+, (2) the corticosterone secretory rates of pregnant and non-pregnant rabbits are controlled mainly by ACTH, and (3) aldosterone secretion by non-pregnant animals is regulated primarily by angiotensin II and secondarily by ACTH and K+, while in pregnant animals ACTH may be the primary regulator of aldosterone secretion as it is in the fetus.

Adrenal Glands↗

PubMed1986

Renal secretion of amino acids in ophidian reptiles.

Net renal tubular secretion of endogenous beta-amino acids (taurine, beta-alanine, beta-aminoisobutyric acid) and their endogenous analogue (L-cysteic acid) was revealed in the olive sea snake, Aipysurus laevis, and in the garter snake, Thamnophis sirtalis, by renal clearance methods. The net secretory rates ranged from 16 to 795 nmol X kg-1 X h-1, with taurine being secreted at the highest rates. These rates of secretion are comparable to those observed in marine fish, the only other group of vertebrates exhibiting renal tubular secretion of L-amino acids under physiological conditions. However, only some snakes (8-58%) demonstrated net tubular secretion; the others (0-58%) showed net tubular reabsorption of these amino acids. Net tubular secretion was consistently observed whenever the filtered load of the amino acid was low, and net reabsorption was apparent whenever the filtered load was high; the two variables being significantly correlated. An analysis of the net amino acid transport rates, both secretory and reabsorptive, as a function of the filtered load suggests that in snakes the beta-amino acids are reabsorbed and secreted at discrete tubular sites, with the secretory sites located beyond the major reabsorptive sites. Taurine, beta-alanine, and L-cysteic acid appear to share a common transport system in the snake renal tubule cells.

Amino Acids↗