The control of adaptive hypertrophy in the salt glands of geese and ducks.

1. Factors controlling adaptive hypertrophy, which occurs when marine, or potentially marine, birds drink salt water, have been investigated in geese and ducks using changes in salt-weight weight, RNA and DNA contents as indices of this process. 2. Unilateral post-ganglionic denervation in geese prevented the changes in [RNA] and [RNA]:[DNA] that occurred in the intact gland of birds given salt water for 24 hr; denervation had no significant effect in birds on fresh water throughout. 3. Atropine treatment also prevented the adaptive changes in geese given salt water. 4. In ducks give 0.3 M-NaCl for 48 hr salt-gland weight, [RNA] and [RNA]:[DNA] increase markedly. Treatment of ducks drinking fresh water with large doses of corticosterone and mammalian ACTH for 48 hr had no significant effects on salt-gland weight, RNA or DNA; mammalian prolactin treatment for 48 hr significantly raised [RNA]. 5. No changes in the total amount of DNA in the glands were observed in these experiments, thus indicating that hyperplasia does not occur within 48 hr of a bird first drinking salt water. 6. It is concluded that adaptive hypertrophy is controlled by secretory nerves, and that hormones, if they play any part in this process, have a permissive or secondary role. It is suggested that hypertrophy and the maintenance of the secretory cells in the fully-adapted state may be obligatorily related to secretory activity induced by cholinergic secretory nerves.

The effects of engorgement with milk and of suckling on mammary blood flow in the rat.

1. Mammary blood flow was estimated in rats by measuring the cardiac output and the proportion of it received by the mammary glands.2. When the young were removed on the 10th day of lactation the mammary glands began to fill with milk and mammary blood flow fell from 78 ml./min. 100 g tissue to 45 ml./min. 100 g within 8 hr and decreased further to 34 ml./min. 100 g within 8 hr and decreased further to 34 ml./min. 100 g in the next 16 hr. These changes were associated with both a fall in cardiac output and a fall in the proportion of the cardiac output taken by the mammary glands.3. When the young were allowed to continue suckling, but milk removal was prevented by sealing the teat ducts with adhesive, more milk collected in the mammary glands within 8 hr and mammary blood flow was unchanged (74 ml./min. 100 g).4. In rats which had been separated from their young for 24 hr, milk was removed from the engorged glands by allowing the pups to suckle again. Mammary blood flow did not rise immediately following the removal of milk but only after 4 hr of suckling, and was associated largely with an increase in cardiac output.5. Upon resumption of suckling mammary blood flow was the same in emptied glands, and in full glands with the teats sealed.6. When the young were removed from 15-day lactating rats mammary blood flow after 24 hr was directly related to the volume of milk in the glands.7. It is concluded that the accumulation of milk in the mammary gland does not mechanically restrict the flow of blood through the tissue and that, in the rat, mammary blood flow and milk secretion are strongly dependent on a continually applied suckling stimulus.

The time course of cardiovascular changes in lactation in the rat.

1. Cardiovascular changes in lactating rats have been traced from the first day post-partum to the end of the third week of lactation. The pattern of changes showed three phases.2. Between days 1 and 5 of lactation there were sharp rises in both cardiac output and in the blood flow/g tissue for most organs, but little change in the distribution of the cardiac output.3. Between days 5 and 15 of lactation cardiac output remained steady. The blood flow to tissues actively involved in the body's response to lactation (mammary glands, liver, gastrointestinal tract) also remained at high steady levels, but the blood flow to other tissues declined due to a redistribution of the cardiac output away from them and towards the growing mammary glands and splanchnic organs.4. Between days 15 and 22 of lactation there were further rises in both cardiac output and in the blood flow/g tissue for most organs.5. It is suggested that the increases in organ blood flows that occurred in the first few days after parturition (days 1-5) and at the end of lactation (days 15-22) were largely dependent on increases in cardiac output and may represent the maternal response to rapidly rising demands from the young at these times.

Nature and location of the receptors for salt-gland secretion in the goose.

1. The nature and location of the receptors which stimulate salt-gland secretion in the goose have been investigated.2. The rapid injection of homologous blood (sufficient to raise the blood volume by 16 and 9%) into the right atrium failed to induce secretion. In contrast, hypertonic sucrose, Na(2)SO(4) and LiCl initiated secretion.3. These results support the theory that osmoreceptors initiate secretion by detecting an increase in plasma tonicity.4. The minimal amount of hypertonic NaCl required to initiate secretion when infusions were made into a carotid artery or into various arteries and veins in the splanchnic region was not less than that required by an I.V. route.5. Cross-circulation and perfusion studies also showed that a raised [NaCl] in the blood perfusing the head was ineffective in evoking secretion and thus that plasma tonicity must be raised elsewhere in the body.6. Secretion in response to salt-loading was abolished or prevented by cutting the vagus nerves or blocking them with local anaesthetic. Stimulation of the cephalic end of the cut vagi in an isolated, perfused decerebrate head induced secretion, indicating that the afferent fibres from the receptors to the C.N.S. lie in the vagus nerves. Cutting the vagi below the heart, however, had no effect on the secretory response.7. Blocking nerves in the crop with local anaesthetic had no effect on secretion induced by salt-loading but when local anaesthetic was injected into the pericardial sac, secretion decreased immediately, stopped, and recovered with a time course similar to that seen after blocking the vagus nerves.8. Section of the vagi in the neck abolished the tachycardia observed in response to the injection of hypertonic NaCl into the right atrium.9. As in other species, stimulation of the ;secretory nerve' induced secretion in anaesthetized or decerebrate geese.10. Hexamethonium given I.V. or applied topically to the ;secretory nerve ganglion' blocked secretion in response to salt-loading or to secretory nerve stimulation.11. It appears that the receptors for salt-gland secretion are located in or near the heart and that afferent fibres from these receptors travel in the vagus nerves to the C.N.S.12. A possible scheme of the secretory reflex which initiates and maintains salt-gland activity is proposed.

Salt-gland secretion and blood flow in the goose.

1. Salt-gland blood flow in the domestic goose has been measured using a combination of Sapirstein's indicator fractionation technique for organ blood flow and Fegler's thermodilution method for cardiac output.2. Nasal salt secretion was induced by giving 0.5 M-NaCl or 0.154 M-NaCl I.V. or by giving artificial sea water by stomach tube into the proventriculus.3. During secretion, salt-gland blood flow increased from 82.7 +/- 21.9 ml./100 g tissue. min to as high as 2179 ml./100 g. min (mean 1209 +/- 140).4. The rate of secretion in response to salt loading was very variable and was not correlated with the rate of blood flow.5. From the data obtained, it could be calculated that the median values for the percentage extraction of ions from the arterial plasma were Na 15%, K 35%, Cl 21% and water 5.8%.6. Atropine abolished secretion but not the increase in blood flow produced by salt loading.7. Unilateral complete denervation abolished secretion from and the increase in blood flow through the operated but not the control gland.8. Anaesthesia, induced by pentobarbitone sodium, almost completely blocked secretion and the increase in blood flow in the salt-gland in response to salt loading.9. In geese given 0.5 or 0.154 M-NaCl I.V. a positive, significant correlation was found between the total amount of nasal secretion collected over 30 min and the concentrations of Na and Cl in the nasal fluid. However, when the time course of secretion was followed in any one bird, the rate of secretion was inversely related to the concentrations of Na and Cl.10. Harderian gland blood flow was not affected by salt loading.

Cardiovascular responses to salt-loading in conscious domestic geese.

1. The intravenous injection of large volumes of 0.5 M-NaCl that are usually used to induce nasal gland secretion in marine birds has been shown in geese to increase greatly plasma volume, cardiac output, heart rate and stroke volume at the time secretion commences after 2-8 min.2. There were no consistent changes in mean arterial blood pressure or in the distribution of the cardiac output to major organs except to the salt-glands whose share increased approximately fourteenfold. Salt-gland blood flow remained high for 10-20 min after cardiac output and heart rate had returned to nearly normal levels.3. The increases in plasma volume and venous return are unlikely to be the stimuli for salt-gland secretion because secretion was also initiated by giving artificial sea water into the proventriculus and this produced no changes in these variables at the time secretion commenced, 5-14 min later.4. At the start of secretion in orally loaded birds, the only detectable changes in the plasma were small increases in osmolality (from 1.3 to 4.6%), Na (from 0.3 to 6%) and Cl (from 1.3 to 7.1%) concentrations.