LakeMountD
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A few people a long time ago asked me why they get such a crazy pump from LR3 IGF-1. Here is your answer.
This also shows a positive effect on blood pressure with IGF-1 use.
Hypertension
Increased IGF-1 mRNA and protein expression in hypertensive aorta and in volume-overloaded caval vein suggests that the IGF-1 axis mediates adaptive growth responses in the vasculature (Table 3).134,135 IGFBP-4 mRNA has been shown to be markedly elevated in the hypertensive rat aorta after abdominal coarctation,136 and this induction of IGFBP-4 is limited to the hypertensive blood vessel. This suggests that increases in vascular load directly stimulate IGFBP-4 expression, and this is consistent with data from Chen et al,137 showing increased IGFBP-2 and BP-4 expression in pressure-overloaded bladder after partial urethral ligation.
The vasoactive effects of IGF-1 indicate that IGF-1 can control blood pressure and regional blood flow via NO. Short-term injection of IGF-1 decreased mean arterial pressure, and this effect was inhibited by preinfusion of an NO inhibitor, indicating that the decrease in blood pressure in response to IGF-1 is mediated by NO.138 A significant elevation of arterial pressure was also observed in mice homozygous for a site-specific insertional mutation in exon 3 of IGF-1.139 Peripheral resistance and systolic blood pressure were increased in liver-specific IGF-1 knockout mice.140 In spontaneously hypertensive rats, IGF-1–induced vasorelaxant effects were impaired before the onset of hypertension, indicating that this effect could play a causative role in the development of hypertension.141 It is of note that smooth muscle–targeted overexpression of IGF-1 results in enhanced vascular contractility, possibly via regulation of contractile protein expression.142
This also shows a positive effect on blood pressure with IGF-1 use.
Hypertension
Increased IGF-1 mRNA and protein expression in hypertensive aorta and in volume-overloaded caval vein suggests that the IGF-1 axis mediates adaptive growth responses in the vasculature (Table 3).134,135 IGFBP-4 mRNA has been shown to be markedly elevated in the hypertensive rat aorta after abdominal coarctation,136 and this induction of IGFBP-4 is limited to the hypertensive blood vessel. This suggests that increases in vascular load directly stimulate IGFBP-4 expression, and this is consistent with data from Chen et al,137 showing increased IGFBP-2 and BP-4 expression in pressure-overloaded bladder after partial urethral ligation.
The vasoactive effects of IGF-1 indicate that IGF-1 can control blood pressure and regional blood flow via NO. Short-term injection of IGF-1 decreased mean arterial pressure, and this effect was inhibited by preinfusion of an NO inhibitor, indicating that the decrease in blood pressure in response to IGF-1 is mediated by NO.138 A significant elevation of arterial pressure was also observed in mice homozygous for a site-specific insertional mutation in exon 3 of IGF-1.139 Peripheral resistance and systolic blood pressure were increased in liver-specific IGF-1 knockout mice.140 In spontaneously hypertensive rats, IGF-1–induced vasorelaxant effects were impaired before the onset of hypertension, indicating that this effect could play a causative role in the development of hypertension.141 It is of note that smooth muscle–targeted overexpression of IGF-1 results in enhanced vascular contractility, possibly via regulation of contractile protein expression.142
