Editing Blood pressure (section)

===Hemodynamics===
{{main|Hemodynamics}}
A simple view of the [[hemodynamics]] of systemic arterial pressure is based around [[mean arterial pressure]] (MAP) and pulse pressure. Most influences on blood pressure can be understood in terms of their effect on [[cardiac output]],<ref>{{cite journal | vauthors = Guyton AC | title = The relationship of cardiac output and arterial pressure control | journal = Circulation | volume = 64 | issue = 6 | pages = 1079–1088 | date = December 1981 | pmid = 6794930 | doi = 10.1161/01.cir.64.6.1079 | doi-access = free }}</ref> [[Vascular resistance|systemic vascular resistance]], or [[arterial stiffness]] (the inverse of arterial compliance). Cardiac output is the product of stroke volume and heart rate. Stroke volume is influenced by 1) the [[end-diastolic volume]] or filling pressure of the ventricle acting via the [[Frank–Starling law|Frank–Starling mechanism]]—this is influenced by [[blood volume]]; 2) [[Myocardial contractility|cardiac contractility]]; and 3) [[afterload]], the impedance to blood flow presented by the circulation.<ref>{{cite journal | vauthors = Milnor WR | title = Arterial impedance as ventricular afterload | journal = Circulation Research | volume = 36 | issue = 5 | pages = 565–570 | date = May 1975 | pmid = 1122568 | doi = 10.1161/01.res.36.5.565 | doi-access = free }}</ref> In the short-term, the greater the blood volume, the higher the cardiac output. This has been proposed as an explanation of the relationship between high dietary salt intake and increased blood pressure; however, responses to increased dietary sodium intake vary between individuals and are highly dependent on autonomic nervous system responses and the [[renin–angiotensin system]],<ref>{{cite journal | vauthors = Freis ED | title = Salt, volume and the prevention of hypertension | journal = Circulation | volume = 53 | issue = 4 | pages = 589–595 | date = April 1976 | pmid = 767020 | doi = 10.1161/01.CIR.53.4.589 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Caplea A, Seachrist D, Dunphy G, Ely D | title = Sodium-induced rise in blood pressure is suppressed by androgen receptor blockade | journal = American Journal of Physiology. Heart and Circulatory Physiology | volume = 280 | issue = 4 | pages = H1793–H1801 | date = April 2001 | pmid = 11247793 | doi = 10.1152/ajpheart.2001.280.4.H1793 | series = 4 | s2cid = 12069178 }}</ref><ref>{{cite journal | vauthors = Houston MC | title = Sodium and hypertension. A review | journal = Archives of Internal Medicine | volume = 146 | issue = 1 | pages = 179–185 | date = January 1986 | pmid = 3510595 | doi = 10.1001/archinte.1986.00360130217028 | series = 1 }}</ref> changes in [[Plasma osmolality|plasma osmolarity]] may also be important.<ref>{{cite journal | vauthors = Kanbay M, Aslan G, Afsar B, Dagel T, Siriopol D, Kuwabara M, Incir S, Camkiran V, Rodriguez-Iturbe B, Lanaspa MA, Covic A, Johnson RJ | display-authors = 6 | title = Acute effects of salt on blood pressure are mediated by serum osmolality | journal = Journal of Clinical Hypertension | volume = 20 | issue = 10 | pages = 1447–1454 | date = October 2018 | pmid = 30232829 | pmc = 8030773 | doi = 10.1111/jch.13374 | doi-access = free }}</ref> In the longer-term the relationship between volume and blood pressure is more complex.<ref>{{cite journal | vauthors = Titze J, Luft FC | title = Speculations on salt and the genesis of arterial hypertension | journal = Kidney International | volume = 91 | issue = 6 | pages = 1324–1335 | date = June 2017 | pmid = 28501304 | doi = 10.1016/j.kint.2017.02.034 | doi-access = free }}</ref> In simple terms, systemic vascular resistance is mainly determined by the caliber of small arteries and arterioles. The resistance attributable to a blood vessel depends on its radius as described by the [[Hagen–Poiseuille equation|Hagen-Poiseuille's equation]]  (resistance∝1/radius<sup>4</sup>). Hence, the smaller the radius, the higher the resistance. Other physical factors that affect resistance include: vessel length (the longer the vessel, the higher the resistance), blood viscosity (the higher the viscosity, the higher the resistance)<ref>{{cite journal | vauthors = Lee AJ | title = The role of rheological and haemostatic factors in hypertension | journal = Journal of Human Hypertension | volume = 11 | issue = 12 | pages = 767–776 | date = December 1997 | pmid = 9468002 | doi = 10.1038/sj.jhh.1000556 | doi-access = free }}</ref> and the number of vessels, particularly the smaller numerous, arterioles and capillaries. The presence of a severe arterial [[stenosis]] increases resistance to flow, however this increase in resistance rarely increases systemic blood pressure because its contribution to total systemic resistance is small, although it may profoundly decrease downstream flow.<ref>{{cite journal | vauthors = Coffman JD | title = Pathophysiology of obstructive arterial disease | journal = Herz | volume = 13 | issue = 6 | pages = 343–350 | date = December 1988 | pmid = 3061915 }}</ref> Substances called [[vasoconstrictor]]s reduce the caliber of blood vessels, thereby increasing blood pressure. [[Vasodilator]]s (such as [[nitroglycerin]]) increase the caliber of blood vessels, thereby decreasing arterial pressure. In the longer term a process termed remodeling also contributes to changing the caliber of small blood vessels and influencing resistance and reactivity to vasoactive agents.<ref>{{cite journal | vauthors = Korner PI, Angus JA | title = Structural determinants of vascular resistance properties in hypertension. Haemodynamic and model analysis | journal = Journal of Vascular Research | volume = 29 | issue = 4 | pages = 293–312 | date = 1992 | pmid = 1391553 | doi = 10.1159/000158945 }}</ref><ref>{{cite journal | vauthors = Mulvany MJ | title = Small artery remodelling in hypertension | journal = Basic & Clinical Pharmacology & Toxicology | volume = 110 | issue = 1 | pages = 49–55 | date = January 2012 | pmid = 21733124 | doi = 10.1111/j.1742-7843.2011.00758.x | doi-access = free }}</ref> Reductions in capillary density, termed capillary rarefaction, may also contribute to increased resistance in some circumstances.<ref>{{cite journal | vauthors = de Moraes R, Tibirica E | title = Early Functional and Structural Microvascular Changes in Hypertension Related to Aging | journal = Current Hypertension Reviews | volume = 13 | issue = 1 | pages = 24–32 | date = 2017 | pmid = 28412915 | doi = 10.2174/1573402113666170413095508 }}</ref>

In practice, each individual's autonomic nervous system and other systems regulating blood pressure, notably the kidney,<ref>{{cite journal | vauthors = Guyton AC, Coleman TG, Cowley AV, Scheel KW, Manning RD, Norman RA | title = Arterial pressure regulation. Overriding dominance of the kidneys in long-term regulation and in hypertension | journal = The American Journal of Medicine | volume = 52 | issue = 5 | pages = 584–594 | date = May 1972 | pmid = 4337474 | doi = 10.1016/0002-9343(72)90050-2 }}</ref> respond to and regulate all these factors so that, although the above issues are important, they rarely act in isolation and the actual arterial pressure response of a given individual can vary widely in the short and long term.