The evolution of blood pressure and the rise of mankind

Schulte, Kevin; Kunter, Uta; Moeller, Marcus J.

doi:10.1093/ndt/gfu275

Cited by 42 publications

(41 citation statements)

References 30 publications

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“…The average capillary surface area per unit volume of tissue is about six times greater in mammals than reptiles. The average diffusion distance between the reptilian capillary and cell is about 2.5 times that in the mammalian system (Pough, ; Schulte et al, ). The reptilian hematocrit is also quite low with an average of 28% and an O 2 capacity of 8.7 ml/100 ml blood for 83+ species tested (Pough, ).…”

Section: Circulatory System/rbcmentioning

confidence: 99%

The role of the red blood cell and platelet in the evolution of mammalian and avian endothermy

Soslau

2019

J Exp Zool Pt B

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This review presents evidence to support the hypothesis that the reduced O2 during the Permian/Triassic period was the impetus for the evolutionary selection of endothermic animals. The evolution of smaller red blood cells with greater surface areas along with increased: capillary density, capillary surface area, hematocrits, blood pressure, blood flow rates, and shear rates were critical for efficient gas exchange in endothermy. The evolution of the four‐chambered mammalian/avian heart allowed for low pulmonary and high systemic blood pressure. It is proposed that hypoxia‐induced angiogenesis led to increased vascularization in endothermic animals. The increased blood pressure, flow rates, and shear forces likely required changes in hemostatic mechanisms that were met in mammals by the evolution of anucleate platelets. The evolution of mammals and birds occurred in a parallel fashion with further genetic changes to anucleate RBCs/platelets occurring in mammals. Although it is possible that the evolution of endothermy in birds and mammals occurred as two independent events, it is more likely that a common ancestor developed genetic mutations that laid down the road map for parallel alterations of their cardiovascular system in response to environmental pressures. Model systems to support the proposed changes from ectotherm to endotherm were developed from published data. The evolutionary development of endothermy occurred over millions of years with a continuum of genetic alterations that involved skeletal, soft tissue, cardiovascular macrochanges along with numerous molecular alterations. Genetic signals and potential regulators for the evolutionary changes of endothermic blood cells from their bipotential stem cells are also proposed.

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Section: Circulatory System/rbcmentioning

confidence: 99%

The role of the red blood cell and platelet in the evolution of mammalian and avian endothermy

Soslau

2019

J Exp Zool Pt B

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“…The appearance of vertebrates, however, with a closed circulation resulted in increased peripheral resistance and higher mean arterial pressure 11 . Since the fibrillin microfibrils alone become very stiff in the context of newly evolved organisms requiring higher perfusion pressure, an increase in pulsatility might have imposed a selection pressure for the evolution of another extra-cellular matrix element required to provide elasticity at higher pressures; this element is tropoelastin 10 .…”

Section: The “Purpose” Of the Aorta: An Evolutionary Perspectivementioning

confidence: 99%

The Conundrum of Arterial Stiffness, Elevated Blood Pressure, and Aging

AlGhatrif

Lakatta²

2015

Curr Hypertens Rep

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Isolated systolic hypertension is a major health burden that is expanding with the aging of our population. There is evidence that central arterial stiffness contributes to the rise in systolic blood pressure (SBP); at the same time central arterial stiffening is accelerated in patients with increased (SBP). This bidirectional relationship created a controversy in the field on whether arterial stiffness leads to hypertension or vice versa. Given the profound interdependency of arterial stiffness and blood pressure, this question seems intrinsically challenging, or probably naïve. The aorta’s function of dampening the pulsatile flow generated by the heart is optimal a range of distending pressure that secures the required distal flow, keeps the aorta in an optimal mechanical conformation, and minimizes cardiac work. This homeostasis is disturbed by age-associated, minute alterations in aortic hemodynamic and mechanical properties that induce short- and long-term alterations in each other. Hence, it is impossible to detect an “initial insult” at an epidemiological level. Earlier manifestations of these alterations are observed in young adulthood with a sharp decline in aortic strain and distensibility accompanied by an increase in diastolic blood pressure. Subsequently aortic mechanical reserve is exhausted, and aortic remodeling with wall stiffening and dilatation ensue. These two phenomena affect pulse pressure in opposite directions and different magnitudes. With early remodeling there is an increase in pulse pressure, due to the dominance of arterial wall stiffness, which in turn accelerates aortic wall stiffness and dilation. With advanced remodeling, which appears to be greater in men, the effect of diameter becomes more pronounced and partially offsets the effect of wall stiffness leading to plateauing in pulse pressure in men, and slower increase in PP than that of wall stiffness in women. The complex nature of hemodynamic changes with aging makes the “one-size-fits-all” approach suboptimal, and urges for therapies that addresses the vascular profile that underlies a given blood pressure, rather than the blood pressure values themselves.

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“…Nevertheless, we agree that the existence, polarity and magnitude of streaming potentials should also be verified in mammalian kidney, which is technically challenging because of the small capillary diameter of these animals with a relatively high blood pressure [17]. Streaming potentials are an entirely novel biophysical phenomenon, and any potential possibility of verifying them is worth the effort.…”

Section: Key Pointsmentioning

confidence: 55%