“
“Please cite this paper as: Sorensen CM, Holstein-Rathlou N-H. Cell–cell

communication in the kidney microcirculation. click here Microcirculation 19: 451–460, 2012. In the renal vasculature of humans, rats, and mice, at least four isoforms of Cx, Cxs 37, 40, 43, and 45 are expressed. In the ECs, Cx40 is the predominantly expressed Cx, whereas Cx45 is suggested to be expressed in the VSMCs. The preglomerular vasculature has a higher expression of Cxs than the postglomerular vasculature. Cxs form gap junctions between neighboring cells, and as in other organ systems, the major function of Cxs in the kidney appears to be mediation of intercellular communication. Cxs may also form hemichannels that allow cellular secretion of signaling molecules like ATP, and thereby mediate paracrine signaling. Renal Cxs facilitate

vascular conduction, juxtaglomerlar apparatus calcium signaling, and enable ECs and VSMCs to communicate. Thus, current research suggests multiple roles for Cxs in important regulatory mechanisms within the kidney, including the renin-angiotensin system, TGF, and salt and water homeostasis. Interestingly, changes in the activity of the renin-angiotensin system or changes in blood pressure seem to affect the expression of the renal vascular Cxs. At the systemic level, renal Cxs may be involved in blood pressure regulation, and possibly in the pathogenesis of hypertension and diabetes. “
“Please cite this paper as: Venetoclax Clough and Norman (2011). The Microcirculation: A Target for Developmental Priming. Microcirculation 18(4), 286–297. There is increasing evidence that the early life environment, of which nutrition is a key component, acts through developmental adaptations to set the capacity of cardiovascular

and metabolic pathways, and ultimately the limits to physiological challenges in later life. Suboptimal maternal nutrition and fetal growth result in reduced microvascular perfusion and functional dilator capacity, which are strongly associated with later development Astemizole of obesity, type 2 diabetes, and hypertension. These conditions are also linked to microvascular rarefaction and remodeling that together limit capillary recruitment, reduce exchange capacity and increase diffusion distances of metabolic substrates, and increase local and overall peripheral resistance. Changes in small vessel structure and function may be seen very early, long before the onset of overt cardiovascular and metabolic disease, and may thus be a target for early therapeutic and lifestyle intervention strategies. This article explores how a disadvantageous microvascular phenotype may result from perinatal priming and how developmental plasticity may become an important and additional risk determinant in susceptibility to cardiometabolic disease in adult life.