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J Buggy

Publications and source records attributed to J Buggy.

44 records · Page 3Linked to original sources
PubMed1971

Metabolic and physical control of cell elongation rate: in vivo studies in nitella.

Several levels of control of elongation rate are revealed through the detailed study of responses of the Nitella internode to abrupt shifts in turgor. The immediate response, which apparently reflects the physical state of the cell, is approximately described by the equation r = (P - Y)m where r is rate, P is pressure, Y is the wall's yielding threshold, and m is related to the wall's apparent fluidity (reciprocal viscosity). Because P and Y are in the range 5 to 6 atmospheres, and (P - Y) is roughly 0.2 atmosphere, elongation rate is initially extremely sensitive to changes in P. A small step-down in turgor (0.7 atmosphere) stops growth, and a similar rise greatly accelerates it. These initial responses are, however, soon (15 minutes) compensated by changes in Y. An apparent metabolism-dependent reaction (azide-sensitive) lowers Y; strain hardening (azide-insensitive) raises it. These two opposing processes, acting on Y, serve as a governor on (P - Y), tending to maintain it at a given value despite changes in P. This ability to compensate is itself a function of turgor. Turgor step-downs are less and less well compensated, leading to lower rate, as turgor falls from 5 atmospheres to about 2 atmospheres where growth appears not to resume. This is the lowest attainable yield value, Y(1). The turgor dependency of compensation reflects a turgor requirement of the Y-lowering ("wall-softening") process. Thus the relation between steady state, r(s), and turgor is an indirect one, derived from time-dependent alterations of the cell wall. This relationship superficially resembles the instantaneously valid one in that, roughly, r(s) = (P - Y(1))m(s). Y(1) and m(s), however, have much lower values than Y and m. The duality of the elongation rate versus turgor relation and the prominent role of Y in regulating rate are the major features of growth control in Nitella.

Journal Article↗
PubMedDate not supplied

Depression of ad lib and angiotensin-induced sodium intake at oestrus.

During the rat oestrous cycle, cholinergic-stimulated water intake is constant across days; while both daily ad lib and angiotensin II-stimulated water intakes are least on the day of oestrus. If permitted to self select, however, rats will elect to drink sodium chloride solutions as well as water under ad lib or angiotensin-stimulated conditions. Therefore, adult female rats with continuous access to both water and 1.8% NaCl were studied to determine if saline intake also varied with the oestrous cycle. Ad lib drinking and drinking stimulated by intracerebroventricular injections of angiotensin II or carbachol were monitored daily for the duration of an entire oestrous cycle. Both ad lib and angiotensin-induced sodium intakes were depressed at oestrus, while the minimal sodium intake seen after carbachol was not changed. The depression in sodium intake so mirrored that observed for water intake that the ratio of saline to water intake did not vary over the oestrous cycle.

Angiotensin II↗
PubMedDate not supplied

Alterations in cerebrospinal fluid sodium and osmolality in rats during one-kidney, one-wrap renal hypertension.

Measurements of plasma and cerebrospinal fluid (CSF) sodium and osmolality were made throughout the course of one-kidney, one-wrap Grollman renal hypertension. Although the plasma sodium and osmolality did not rise after 28 days, CSF sodium and osmolality was increased significantly at 3 days postwrap. As a result, the CSF to plasma ratio for both sodium and osmolality was significantly elevated during the initial postwrap period. These observations suggest that an increase in CSF sodium may provide an initiating stimulus for an elevated arterial pressure in one-kidney, one-wrap renal hypertension.

Animals↗
PubMedDate not supplied

Interruption of the maintenance phase of established hypertension by ablation of the anteroventral third ventricle (AV3V) in rats.

Ablation of tissue surrounding anteroventral third ventricle (AV3V) was studied in three models of hypertensive rats. Lesions were placed in the AV3V at one and six weeks following the initiation of one kidney Grollman renal hypertension. At one week the rise in blood pressure was arrested and water intake was reduced; at six weeks arterial pressure returned to prehypertensive levels in animals surviving the post-lesion hydrational crisis. In two kidney (one clip) Goldblatt animals lesioned two weeks post-clip, arterial pressure was significantly reduced but did not become fully normotensive. Finally, the AV3V was also lesioned in spontaneously hypertensive rats (SHR-Okamoto strain) with established hypertension. The lesion did not reduce arterial pressure in adult SHR although characteristic initial adipsia and weight loss occurred. Ablation of the AV3V thus altered the course of maintenance of renal hypertension; however, the arterial pressure of SHR was not affected.

Animals↗