The cell reproduction cycle of parasitic wall-free bacteria, mycoplasma, is reviewed. DNA replication of Mycoplasma capricolum starts at a fixed site neighboring the dnaA gene and proceeds to both directions after a short arrest in one direction. The initiation frequency fits to the slow speed of replication fork and DNA content is set constant. The replicated chromosomes migrate to one and three quarters of cell length before cell division to ensure delivery of the replicated DNA to daughter cells. The cell reproduction is based on binary fission but a branch is formed when DNA replication is inhibited. Mycoplasma pneumoniae has a terminal structure, designated as an attachment organelle, responsible for both host cell adhesion and gliding motility. Behavior of the organelle in a cell implies coupling of organelle formation to the cell reproduction cycle. Several proteins coded in three operons are delivered sequentially to a position neighboring the previous organelle and a nascent one is formed. One of the duplicated attachment organelles migrates to the opposite pole of the cell before cell division. It is becoming clear that mycoplasmas have specialized cell reproduction cycles adapted to the limited genome information and parasitic life.

Bacterial Adhesion↗

PubMedDate not supplied

Dynamic responses of active and inactive renin in patients with essential and renovascular hypertension.

We studied the dynamic responses of inactive renin and the form of renin released by the kidney in the hypertensive patients. Significant increase of active renin concentration (p less than 0.01) and decrease of the percentage of inactive renin concentration (p less than 0.01) after sodium depletion was observed in 15 essential hypertensive subjects with normal plasma renin activity. In eight of 15 patients, significant increase of inactive renin concentration (p less than 0.01) was observed after sodium depletion. In the remaining seven patients, no significant change of inactive renin concentration was demonstrated. A small increase of active and inactive renin concentration was observed following sodium depletion in six essential hypertensive subjects with low plasma renin activity (PRA). In the unilateral renal hypertension after upright tilting, active renin concentration in the renal vein of the affected kidney was significantly (p less than 0.02) higher than that in the renal vein of the non-affected kidney and the inferior vena cava. Inactive renin concentration in the renal vein of the affected kidney was significantly (p less than 0.02) lower than that in the renal vein of the nonaffected kidney and the inferior vena cava. In four of five cases, the inactive renin concentration in the femoral artery was less than that in the inferior vena cava. Therefore, we might conclude that only active renin was released from the affected kidney, and active renin became inactive by unknown mechanisms; the ischemic kidney might also activate inactive renin.

Adolescent↗

PubMedDate not supplied

The effect of aprotinin (a serine protease inhibitor) on renal function and renin release.

We studied the effect of aprotinin, a reversible inhibitor of kallikrein and other serine proteases, upon urinary kallikrein and kinin excretion, renal function and hemodynamics, blood pressure, and plasma renin activity (PRA). When aprotinin was administered to anesthetized rats at 10,000 KIU/kg as a bolus, and at 1000 KIU/kg/min infusion for 60 minutes, urinary kininogenase activity and immunoreactive kallikrein, kinins, sodium, potassium, and water excretion, and PRA decreased significantly. Aprotinin also caused a 36% decrease (p less than 0.001) in renal blood flow (RBF), and a 37% decrease (p less than 0.001) in glomerular filtration rate (GFR), although neither blood pressure nor cardiac output changed. The effect of aprotinin on PRA was further studied in conscious rats before and after stimulation of renin release by isoproterenol or furosemide. Aprotinin (5,000 KIU/kg bolus and 1000 KIU/kg/min infusion for 60 minutes) did not alter basal or isoproterenol-stimulated PRA, but it blunted the increase in PRA as stimulated by furosemide. Aprotinin at a higher dose (20,000 KIU/kg bolus and 5000 KIU/kg/min infusion for 60 minutes) significantly lowered blood pressure and increased hematocrit and PRA. These effects may be due to inhibition of serine protease(s) or to other as yet unrecognized properties of this peptide resulting from its highly cationic nature. In conclusion, aprotinin at a low dose decreased kallikrein, kinin, sodium, and water excretion. These decreases may be due to the inhibition of kallikrein and/or other serine proteases or may be secondary to the renal hemodynamic changes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗