Search

This paper presents the design of a four-legged walking machine with a versatile leg construction. It offers the possibility to investigate reptile- and mammal-like walking with only one mechanical realization. A flexible spine will support walking with better stability. For the control of the machine, a hierarchical organized control hardware will be used, which has been very successful on our other walking machines.

Angiotensin II (ANG II) reversibly depolarizes renin-containing juxtaglomerular epithelioid cells (JGECs) of the hydronephrotic mouse kidney afferent arteriole. This depolarizing response was utilized to assess changes in ANG II concentration in the vicinity of JGECs in order to test whether ANG II is generated from ANG I and artificial renin substrate (ARS) in this preparation. Depolarizations were also produced by the application of ANG I and ARS in the superfusing medium. These responses to ANG I and ARS were completely blocked by saralasin. Hence, our findings are indicative for an intrarenal, local generation of ANG II. As opposed to saralasin, several converting enzyme and renin inhibitors only diminished but generally did not abolish the actions of ANG I and ARS, respectively. These results suggest an alternative, nonrenin and non-converting enzyme-dependent pathway of ANG II generation in renal tissue.

In several studies in vivo, atrial natriuretic peptides(ANP) did either not affect (1,2) or induced a moderate decrease(3,4) of renin secretion from the kidney or plasma renin concentrations. In these studies, ANP produced significant changes of systemic and intrarenal hemodynamics and renal tubular function, all of which are known to participate in the control of renin secretion. It therefore remained unclear, whether ANPs have any direct effect on renin secreting juxtaglomerular cells. We have therefore examined the influence of atrial natriuretic peptide on renin secretion from the isolated rat kidney, in which interference by neuronal, hemodynamic, humoral, and, to some extent, also tubular mechanisms can be excluded. Part of the results have been published in preliminary form(5).

Intracellular recordings were made in juxtaglomerular granulated (JG) cells and in vascular smooth muscle (VSM) cells in afferent arterioles of hydronephrotic mouse kidneys. Both cell types did not differ in their passive and active electrical membrane properties; membrane potential was about -58 mV, input resistance exceeded 400 M omega, and JG as well as VSM cells showed spontaneous depolarizations resembling excitatory junction potentials and active responses observed in smooth muscle cells of other blood vessels in various species. These depolarizations, attributed to spontaneous transmitter release from adrenergic terminals, were extremely polymorphous and quite frequent. Epinephrine, norepinephrine, phenylephrine, arginine vasopressin, and angiotensin II depolarized JG and VSM cells, but isoproterenol and orciprenaline had no effect. A hyperpolarizing action of catecholamines was never observed. It is suggested that, in this in vitro preparation, isoproterenol increases renin secretion by a mechanism independent of membrane potential changes. Depolarizations mediated by alpha-mimetic agents, arginine vasopressin, and angiotensin II, as well as by the junctional activity may inhibit renin secretion by an increased calcium influx into JG cells.