Preserving cell shape under environmental stress

Maintaining cell shape and tone is crucial for the function and survival of cells and tissues. Mechanotransduction relies on the transformation of minuscule mechanical forces into high-fidelity electrical responses. When mechanoreceptors are stimulated, mechanically sensitive cation channels open and produce an inward transduction current that depolarizes the cell. For this process to operate effectively, the transduction machinery has to retain integrity and remain unfailingly independent of environmental changes. This is particularly challenging for poikilothermic organisms, where changes in temperature in the environment may impact the function of mechanoreceptor neurons. Thus, we wondered how insects whose habitat might quickly vary over several tens of degrees of temperature manage to maintain highly effective mechanical senses. We screened for Drosophila mutants with defective mechanical responses at elevated ambient temperatures, and identified a gene, spam, whose role is to protect the mechanosensory organ from massive cellular deformation caused by heat-induced osmotic imbalance. Here we show that Spam protein forms an extracellular shield that guards mechanosensory neurons from environmental insult. Remarkably, heterologously expressed Spam protein also endowed other cells with superb defence against physically and chemically induced deformation. We studied the mechanical impact of Spam coating and show that spam-coated cells are up to ten times stiffer than uncoated controls. Together, these results help explain how poikilothermic organisms preserve the architecture of critical cells during environmental stress, and illustrate an elegant and simple solution to such challenge.     

Plasma angiotensin,serum ‘angiotensinase activity’, and blood pressure response during angiotensin II amide infusions in normal volunteers

Résumé Des doses croissantes d'angiotensine II amide furent injectées à des volontaires normaux. La réponse de la pression artérielle fut en relation directe avec le log de la dose de peptide injectée, avec la concentration sérique en sodium et avec l'activité sérique «angiotensinase», mais en relation inverse avec l'augmentation de la concentration plasmatique en angiotensine. Ces résultats suggèrent que la réponse de pression est déterminée, au moins en partie, par le «turnover» du peptide au niveau des récepteurs et qu'à ce niveau angiotensinase influence le «turnover» et la concentration plasmatique du peptide.

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A preliminary report of this work was presented at the Eastern Section Meeting of the American Federation for Clinical Research, Washington, D.C., December 13, 1969.

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Supported by U.S.P.H.S. Grant No. HE 11691-02, NIH; the American and Maryland Heart Associations; and the Kidney Foundation of Maryland. Thanks are due Dr.J. R. Hebel for statistical analyses and MissD. S. Baker for secretarial assistance.

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Supported by the Fulbright-Hays Program and the Italian National Research Council.     

Hypothyroidism lowers blood pressure,adenylate cyclase and Na+, K+-and K+, Ca++-ATPase activities in normotensive and spontaneously hypertensive rats

Summary Myocardial isoproterenol-stimulated adenylate cyclase, Na⁺, K⁺-ATPase and K⁺, Ca⁺⁺-ATPase activities are elevated in the spontaneously hypertensive rat and can be lowered by methimazole-induced hypothyroidism which also prevents the development of hypertension. Although thyroid hormone levels are similar between untreated SHRs and WKY rats, the thyroid is apparently necessary for the expression of spontaneous hypertension.Acknowledgments. Supported by North Carolina Heart Grant No. 40301 and a grant from Sigma Xi.